This document defines vitamins and classifies them as either water soluble or fat soluble. It then discusses the vitamin thiamine (vitamin B1) in detail. Thiamine acts as a coenzyme in carbohydrate metabolism and energy production. Deficiency results in beriberi disease. The document also covers the structure, functions, deficiency and food sources of riboflavin (vitamin B2).
A vitamin that can dissolve in water. Vitamins are nutrients that the body needs in small amounts to stay healthy and work the way it should. Water-soluble vitamins are carried to the body's tissues but are not stored in the body.
Biochemistry of Vitamins for Medical Students-RajendraRajendra Dev Bhatt
Vitamins are organic compounds that are essential nutrients required in small amounts for normal physiological functions. They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Vitamins act as coenzymes and play important roles in metabolism. Deficiencies can result from inadequate intake or absorption and cause diseases like beriberi (B1), pellagra (B3), and scurvy (C).
This document provides information about vitamins, including their classification, sources, functions, and deficiency diseases. It discusses both fat-soluble vitamins A, D, E, and K and water-soluble B vitamins and vitamin C. Vitamins are organic compounds that are needed in small amounts for growth, cell function, and disease prevention. They are classified based on their solubility and whether they can be stored in the body. Deficiencies can result in diseases like rickets, osteomalacia, and beriberi.
Medical Biochemistry | Food and Nutrition, Vitamins and Minerals: Water Solub...MarufaAkhter2
This is a lecture class presentation for the students of Medical Biochemistry on the water-soluble vitamin - vitamin B1, its dietary sources, co-enzyme forms, chemical structure, functions, deficiency diseases, and their prevention and treatments.
This document provides information on vitamins, including their definition, classification, importance, and specific details about fat-soluble and water-soluble vitamins. Some key points:
- Vitamins are organic compounds needed in small amounts that must be obtained through diet as they are not synthesized by the body.
- They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Fat-soluble vitamins are absorbed with fat and stored in liver while water-soluble vitamins dissolve in water and are not stored.
- Vitamins play important roles as coenzymes and precursors for biochemical reactions involved in growth, metabolism and disease
This document provides information on vitamins, including their definition, classification, importance, and specific details about fat-soluble and water-soluble vitamins. Some key points:
- Vitamins are organic compounds needed in small amounts that must be obtained through diet as they are not synthesized by the body.
- They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Fat-soluble vitamins are absorbed with fat and stored in liver while water-soluble vitamins dissolve in water and are not stored.
- Vitamins play important roles as coenzymes and precursors for biochemical reactions involved in growth, tissue maintenance,
This document defines vitamins and classifies them as either water soluble or fat soluble. It then discusses the vitamin thiamine (vitamin B1) in detail. Thiamine acts as a coenzyme in carbohydrate metabolism and energy production. Deficiency results in beriberi disease. The document also covers the structure, functions, deficiency and food sources of riboflavin (vitamin B2).
A vitamin that can dissolve in water. Vitamins are nutrients that the body needs in small amounts to stay healthy and work the way it should. Water-soluble vitamins are carried to the body's tissues but are not stored in the body.
Biochemistry of Vitamins for Medical Students-RajendraRajendra Dev Bhatt
Vitamins are organic compounds that are essential nutrients required in small amounts for normal physiological functions. They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Vitamins act as coenzymes and play important roles in metabolism. Deficiencies can result from inadequate intake or absorption and cause diseases like beriberi (B1), pellagra (B3), and scurvy (C).
This document provides information about vitamins, including their classification, sources, functions, and deficiency diseases. It discusses both fat-soluble vitamins A, D, E, and K and water-soluble B vitamins and vitamin C. Vitamins are organic compounds that are needed in small amounts for growth, cell function, and disease prevention. They are classified based on their solubility and whether they can be stored in the body. Deficiencies can result in diseases like rickets, osteomalacia, and beriberi.
Medical Biochemistry | Food and Nutrition, Vitamins and Minerals: Water Solub...MarufaAkhter2
This is a lecture class presentation for the students of Medical Biochemistry on the water-soluble vitamin - vitamin B1, its dietary sources, co-enzyme forms, chemical structure, functions, deficiency diseases, and their prevention and treatments.
This document provides information on vitamins, including their definition, classification, importance, and specific details about fat-soluble and water-soluble vitamins. Some key points:
- Vitamins are organic compounds needed in small amounts that must be obtained through diet as they are not synthesized by the body.
- They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Fat-soluble vitamins are absorbed with fat and stored in liver while water-soluble vitamins dissolve in water and are not stored.
- Vitamins play important roles as coenzymes and precursors for biochemical reactions involved in growth, metabolism and disease
This document provides information on vitamins, including their definition, classification, importance, and specific details about fat-soluble and water-soluble vitamins. Some key points:
- Vitamins are organic compounds needed in small amounts that must be obtained through diet as they are not synthesized by the body.
- They are classified as either fat-soluble (A, D, E, K) or water-soluble (B complex, C). Fat-soluble vitamins are absorbed with fat and stored in liver while water-soluble vitamins dissolve in water and are not stored.
- Vitamins play important roles as coenzymes and precursors for biochemical reactions involved in growth, tissue maintenance,
Vitamins & vitamin containing drugs manikImran Nur Manik
Vitamins are organic compounds that are essential nutrients for the human body. There are 13 essential vitamins that must be obtained through diet as the body cannot synthesize them. Vitamins play important roles in growth, development, and metabolic processes. Deficiencies can lead to specific diseases. Vitamins can be fat-soluble like A, D, E and K which are stored in the body, or water-soluble like the B vitamins and C which are not stored. Dietary sources and functions of several key vitamins are discussed.
Nutrition refers to the process by which living organisms take in and metabolize food to build tissue and liberate energy. The study of human and animal food and liquid requirements for normal physiological functions is called nutrition. Food composition determines appearance, feelings, thoughts, and behaviors. Food contains nutrients like proteins, carbohydrates, fats, minerals, and vitamins that are essential for growth and functioning. Deficiencies in proteins, fats, carbohydrates, vitamins, or minerals can lead to various health issues. Certain diets can help reduce risks of diseases like coronary heart disease, hypertension, dental caries, diabetes, and some cancers.
This document discusses vitamins, coenzymes, and their roles and importance. It defines vitamins as organic compounds needed for normal metabolic processes and growth. Vitamins cannot be produced by the body and must be obtained through diet. The document then discusses various B vitamins (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folic acid, cobalamin) and their functions, sources, and deficiency diseases. It also covers fat-soluble vitamins A, D, E, K and water-soluble vitamin C, describing their structures, roles, sources, and what deficiencies cause. Finally, it provides an overview of coenzymes
This document provides information on nutrients and their functions in the human body. It discusses the six categories of nutrients - macronutrients (carbohydrates, proteins, fats) and micronutrients (vitamins, minerals). Each nutrient is described in terms of its functions, dietary sources, and the effects of deficiency and excess. The document aims to educate on essential substances required for growth, development, and maintenance of health.
This document provides information on nutrients and their functions in the human body. It discusses the six categories of nutrients - macronutrients (carbohydrates, proteins, fats) and micronutrients (vitamins, minerals). Each nutrient is described in terms of its functions, dietary sources, and the effects of deficiency and excess. The document aims to educate on essential substances required for growth, development, and maintenance of health.
This document discusses vitamins, specifically vitamin A. It defines vitamins and explains that vitamin A has several important functions in the body related to vision, epithelial cell integrity, immune response, reproduction and growth. It describes the different forms of vitamin A found in foods and how they are absorbed and transported. Deficiency and toxicity of vitamin A are outlined as well as recommended intake amounts and treatment. The key functions and food sources of vitamin A are summarized.
The document outlines the key nutritional requirements for humans, including calories, essential amino acids, fatty acids, vitamins, and minerals. It then discusses common nutritional deficiencies like marasmus and kwashiorkor that result from insufficient calorie or protein intake. The document also covers overnutrition issues like obesity and examines the role of fiber, protein, fats, cholesterol, and vitamins/minerals in the human diet.
The document discusses water soluble vitamins. It notes that ten vitamins including ascorbic acid, bioflavonoids, and the B vitamins are water soluble. These vitamins are not readily stored by the body and deficiencies can occur quickly if not obtained from the diet. The B vitamins, also called the B complex vitamins, are involved in energy production and hematopoiesis. They are mainly found in plant foods like cereal grains, flour, bran and yeast. Exceptions include leafy greens as a good source of folic acid and foods like meat, fish and dairy being good sources of vitamin B12. The document then discusses specific B vitamins like thiamine, riboflavin and their roles in biochemical processes.
This document summarizes key aspects of several water-soluble vitamins, including their functions, absorption, clinical deficiencies, food sources, and uses for supplementation. It discusses the vitamins thiamine, riboflavin, niacin, pyridoxine, folic acid, and vitamin C, describing how each acts as a coenzyme in important metabolic processes and what health issues can result from deficiencies. Food sources rich in each vitamin are also outlined, as well as therapeutic uses for supplementation.
A Comprehensive Introduction to Vitamins and its chemistry, source, RDA, classification, deficiency states and biological importance. This will give readers a overall insight to this topic.
This document summarizes key vitamins and their functions. It discusses both fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (C, B-complex). Each vitamin is described in terms of its chemical properties, functions in the body, dietary sources, and deficiency symptoms. The B-complex vitamins include thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7), folic acid (B9), and cobalamin (B12).
This document summarizes key vitamins and their functions. It discusses both fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (C, B-complex). Each vitamin is described in terms of its chemical properties, functions in the body, food sources, and deficiency symptoms. The document provides a comprehensive overview of the essential vitamins needed for human health.
The Clinical Nutrition Service is responsible for advising and adapting diets for various disease conditions to hospitalized patients or patients visiting outpatient clinics. The staff of the unit includes clinical nutritionists qualified in various fields of specialization such as: diabetes, gestational diabetes, digestive system diseases, geriatrics, surgery and heart, among others.
This document discusses vitamin B1 (thiamine). It defines vitamins and provides information on the chemistry, dietary sources, deficiency symptoms, and physiological significance of vitamin B1. Key points include: vitamin B1 enables the body to use carbohydrates as energy and plays a role in nerve, muscle, and heart function; common dietary sources include cereals, pulses, nuts, and pork; deficiency can cause beri-beri and symptoms like weakness; and the active form, thiamine pyrophosphate, is important for glucose metabolism and energy releasing reactions.
This document provides information on water soluble vitamins B and C. It discusses the classification of vitamins based on solubility and describes key features of the B-complex vitamins including thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folic acid, and cyanocobalamin. It also covers vitamin C, describing its isolation, sources, functions, deficiency manifestations, and role in collagen formation and wound healing. The roles of these vitamins as coenzymes in various metabolic pathways are emphasized.
The document discusses the composition of an adequate diet and nutrition. It defines nutrition as the utilization of foods by living organisms through biochemical processes. Human nutrition can be undernutrition, optimal nutrition, or overnutrition. Nutrients are the ingredients in food needed for normal body functioning and provide energy through macronutrients like proteins, carbohydrates, and fats or micronutrients like vitamins and minerals. An adequate diet supplies these nutrients, along with dietary fiber and water. The energy and nutrient needs of individuals vary based on factors like age, sex, weight, activity level, pregnancy, and lactation. Both undernutrition and overnutrition can impact health.
Vitamins and minerals are essential micronutrients that serve important functions in the body. Vitamins are organic compounds needed in small amounts that can be divided into water and fat soluble categories. Minerals are inorganic elements that are classified as major or trace minerals needed for processes like bone and tissue formation. The document provides details on the functions, sources, and deficiency effects of important vitamins like A, D, C and B vitamins and minerals like calcium, iron, and iodine. Fortification of foods can help address micronutrient deficiencies in populations.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
More Related Content
Similar to Vitamins .......,..............................
Vitamins & vitamin containing drugs manikImran Nur Manik
Vitamins are organic compounds that are essential nutrients for the human body. There are 13 essential vitamins that must be obtained through diet as the body cannot synthesize them. Vitamins play important roles in growth, development, and metabolic processes. Deficiencies can lead to specific diseases. Vitamins can be fat-soluble like A, D, E and K which are stored in the body, or water-soluble like the B vitamins and C which are not stored. Dietary sources and functions of several key vitamins are discussed.
Nutrition refers to the process by which living organisms take in and metabolize food to build tissue and liberate energy. The study of human and animal food and liquid requirements for normal physiological functions is called nutrition. Food composition determines appearance, feelings, thoughts, and behaviors. Food contains nutrients like proteins, carbohydrates, fats, minerals, and vitamins that are essential for growth and functioning. Deficiencies in proteins, fats, carbohydrates, vitamins, or minerals can lead to various health issues. Certain diets can help reduce risks of diseases like coronary heart disease, hypertension, dental caries, diabetes, and some cancers.
This document discusses vitamins, coenzymes, and their roles and importance. It defines vitamins as organic compounds needed for normal metabolic processes and growth. Vitamins cannot be produced by the body and must be obtained through diet. The document then discusses various B vitamins (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folic acid, cobalamin) and their functions, sources, and deficiency diseases. It also covers fat-soluble vitamins A, D, E, K and water-soluble vitamin C, describing their structures, roles, sources, and what deficiencies cause. Finally, it provides an overview of coenzymes
This document provides information on nutrients and their functions in the human body. It discusses the six categories of nutrients - macronutrients (carbohydrates, proteins, fats) and micronutrients (vitamins, minerals). Each nutrient is described in terms of its functions, dietary sources, and the effects of deficiency and excess. The document aims to educate on essential substances required for growth, development, and maintenance of health.
This document provides information on nutrients and their functions in the human body. It discusses the six categories of nutrients - macronutrients (carbohydrates, proteins, fats) and micronutrients (vitamins, minerals). Each nutrient is described in terms of its functions, dietary sources, and the effects of deficiency and excess. The document aims to educate on essential substances required for growth, development, and maintenance of health.
This document discusses vitamins, specifically vitamin A. It defines vitamins and explains that vitamin A has several important functions in the body related to vision, epithelial cell integrity, immune response, reproduction and growth. It describes the different forms of vitamin A found in foods and how they are absorbed and transported. Deficiency and toxicity of vitamin A are outlined as well as recommended intake amounts and treatment. The key functions and food sources of vitamin A are summarized.
The document outlines the key nutritional requirements for humans, including calories, essential amino acids, fatty acids, vitamins, and minerals. It then discusses common nutritional deficiencies like marasmus and kwashiorkor that result from insufficient calorie or protein intake. The document also covers overnutrition issues like obesity and examines the role of fiber, protein, fats, cholesterol, and vitamins/minerals in the human diet.
The document discusses water soluble vitamins. It notes that ten vitamins including ascorbic acid, bioflavonoids, and the B vitamins are water soluble. These vitamins are not readily stored by the body and deficiencies can occur quickly if not obtained from the diet. The B vitamins, also called the B complex vitamins, are involved in energy production and hematopoiesis. They are mainly found in plant foods like cereal grains, flour, bran and yeast. Exceptions include leafy greens as a good source of folic acid and foods like meat, fish and dairy being good sources of vitamin B12. The document then discusses specific B vitamins like thiamine, riboflavin and their roles in biochemical processes.
This document summarizes key aspects of several water-soluble vitamins, including their functions, absorption, clinical deficiencies, food sources, and uses for supplementation. It discusses the vitamins thiamine, riboflavin, niacin, pyridoxine, folic acid, and vitamin C, describing how each acts as a coenzyme in important metabolic processes and what health issues can result from deficiencies. Food sources rich in each vitamin are also outlined, as well as therapeutic uses for supplementation.
A Comprehensive Introduction to Vitamins and its chemistry, source, RDA, classification, deficiency states and biological importance. This will give readers a overall insight to this topic.
This document summarizes key vitamins and their functions. It discusses both fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (C, B-complex). Each vitamin is described in terms of its chemical properties, functions in the body, dietary sources, and deficiency symptoms. The B-complex vitamins include thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7), folic acid (B9), and cobalamin (B12).
This document summarizes key vitamins and their functions. It discusses both fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (C, B-complex). Each vitamin is described in terms of its chemical properties, functions in the body, food sources, and deficiency symptoms. The document provides a comprehensive overview of the essential vitamins needed for human health.
The Clinical Nutrition Service is responsible for advising and adapting diets for various disease conditions to hospitalized patients or patients visiting outpatient clinics. The staff of the unit includes clinical nutritionists qualified in various fields of specialization such as: diabetes, gestational diabetes, digestive system diseases, geriatrics, surgery and heart, among others.
This document discusses vitamin B1 (thiamine). It defines vitamins and provides information on the chemistry, dietary sources, deficiency symptoms, and physiological significance of vitamin B1. Key points include: vitamin B1 enables the body to use carbohydrates as energy and plays a role in nerve, muscle, and heart function; common dietary sources include cereals, pulses, nuts, and pork; deficiency can cause beri-beri and symptoms like weakness; and the active form, thiamine pyrophosphate, is important for glucose metabolism and energy releasing reactions.
This document provides information on water soluble vitamins B and C. It discusses the classification of vitamins based on solubility and describes key features of the B-complex vitamins including thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folic acid, and cyanocobalamin. It also covers vitamin C, describing its isolation, sources, functions, deficiency manifestations, and role in collagen formation and wound healing. The roles of these vitamins as coenzymes in various metabolic pathways are emphasized.
The document discusses the composition of an adequate diet and nutrition. It defines nutrition as the utilization of foods by living organisms through biochemical processes. Human nutrition can be undernutrition, optimal nutrition, or overnutrition. Nutrients are the ingredients in food needed for normal body functioning and provide energy through macronutrients like proteins, carbohydrates, and fats or micronutrients like vitamins and minerals. An adequate diet supplies these nutrients, along with dietary fiber and water. The energy and nutrient needs of individuals vary based on factors like age, sex, weight, activity level, pregnancy, and lactation. Both undernutrition and overnutrition can impact health.
Vitamins and minerals are essential micronutrients that serve important functions in the body. Vitamins are organic compounds needed in small amounts that can be divided into water and fat soluble categories. Minerals are inorganic elements that are classified as major or trace minerals needed for processes like bone and tissue formation. The document provides details on the functions, sources, and deficiency effects of important vitamins like A, D, C and B vitamins and minerals like calcium, iron, and iodine. Fortification of foods can help address micronutrient deficiencies in populations.
Similar to Vitamins .......,.............................. (20)
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
2. Learning Objectives
Define, classify vitamins and enumerate the difference
between fat soluble and water soluble vitamins
Describe the metabolism, biochemical functions,
deficiency diseases associated with inadequate intake,
and toxicity of excessive intakes of the vitamins
Learning Objectives
Define, classify vitamins and enumerate the difference
between fat soluble and water soluble vitamins
Describe the metabolism, biochemical functions,
deficiency diseases associated with inadequate intake,
and toxicity of excessive intakes of the vitamins
3. Definition and classification of vitamins
Vitamins are organic nutrients that are required in small
quantities for a variety of biochemical functions and
which generally cannot be synthesized by the body and
must, therefore, be supplied by the diet.
Some vitamins can be synthesized by intestinal
microorganisms, but in quantities that are not sufficient to
meet our needs.
Definition and classification of vitamins
Vitamins are organic nutrients that are required in small
quantities for a variety of biochemical functions and
which generally cannot be synthesized by the body and
must, therefore, be supplied by the diet.
Some vitamins can be synthesized by intestinal
microorganisms, but in quantities that are not sufficient to
meet our needs.
4. Classification of vitamins
1. Water soluble vitamins
2. Fat soluble vitamins
Classification of vitamins
1. Water soluble vitamins
2. Fat soluble vitamins
5. Water soluble vitamins
Vitamin B complex, e.g.
– Thiamine (vitamin B1)
– Riboflavin (vitamin B2)
– Niacin (vitamin B3)
– Pantothenic acid (vitamin B5)
– Pyridoxine (vitamin B6)
– Biotin
– Folic acid
– Cobalamin (vitamin B12)
Vitamin C or ascorbic acid.
Water soluble vitamins
Vitamin B complex, e.g.
– Thiamine (vitamin B1)
– Riboflavin (vitamin B2)
– Niacin (vitamin B3)
– Pantothenic acid (vitamin B5)
– Pyridoxine (vitamin B6)
– Biotin
– Folic acid
– Cobalamin (vitamin B12)
Vitamin C or ascorbic acid.
6. Fat soluble vitamins
– Vitamin A or retinol
– Vitamin D or cholecalciferol
– Vitamin E or tocopherol
– Vitamin K.
Fat soluble vitamins
– Vitamin A or retinol
– Vitamin D or cholecalciferol
– Vitamin E or tocopherol
– Vitamin K.
7. Fat Soluble Vs. Water Soluble Vitamins
Fat soluble vitamins Water soluble vitamins
Function as coenzymes,
hormones and
antioxidants
Function as precursor for
coenzymes and
antioxidants
Function as coenzymes,
hormones and
antioxidants
Function as precursor for
coenzymes and
antioxidants
Toxic when taken in
excessive quantities
Usually non-toxic
Can be stored Not stored extensively
except vitamin B12,
8. Thiamine (Vitamin B1)
Thiamine consists of a pyrimidine ring attached to a thiazole
ring by methylene bridge.
Structure of thiamin.
9. Active Form of Thiamine
Thiamine pyrophosphate (TPP) is an active coenzyme
form of vitamin thiamine
10. Sources
It is present in all natural foods but particularly good
dietary sources are unrefined cereals, meat, nuts, green
vegetables, eggs, etc.
White bread and polished rice are very poor sources of
the vitamin thiamine.
Sources
It is present in all natural foods but particularly good
dietary sources are unrefined cereals, meat, nuts, green
vegetables, eggs, etc.
White bread and polished rice are very poor sources of
the vitamin thiamine.
11. Functions
Thiamine is required mainly for carbohydrate
metabolism
Thiamine pyrophosphate (TPP) is a coenzyme involved
in oxidative decarboxylation and transketolase
reactions .
Functions
Thiamine is required mainly for carbohydrate
metabolism
Thiamine pyrophosphate (TPP) is a coenzyme involved
in oxidative decarboxylation and transketolase
reactions .
12. 1. Oxidative Decarboxylation
TPP is a coenzyme for pyruvate dehydrogenase complex
which catalyzes the conversion of pyru- vate into acetyl
CoA.
Acetyl-CoA is a precursor for the synthesis of
neurotransmitter acetylcholine and also for the synthesis
of myelin. Thus, thiamine is required for the normal
functioning of the nervous system.
1. Oxidative Decarboxylation
TPP is a coenzyme for pyruvate dehydrogenase complex
which catalyzes the conversion of pyru- vate into acetyl
CoA.
Acetyl-CoA is a precursor for the synthesis of
neurotransmitter acetylcholine and also for the synthesis
of myelin. Thus, thiamine is required for the normal
functioning of the nervous system.
13. 2. TPP is a coenzyme for α-ketoglutarate dehydro- genase
which catalyzes the conversion of α-ketoglutarate to
succinyl-CoA in TCA cycle
3. TPP is a coenzyme for the enzyme transketolase, in the
pentose phosphate pathway of glucose oxidation
2. TPP is a coenzyme for α-ketoglutarate dehydro- genase
which catalyzes the conversion of α-ketoglutarate to
succinyl-CoA in TCA cycle
3. TPP is a coenzyme for the enzyme transketolase, in the
pentose phosphate pathway of glucose oxidation
14. Nutritional Requirements
Nutritional Research Council recommends daily intake
of 1.0 to 1.5 mg of thiamine for adults which is increased
with increased muscular activity, dietary carbohydrates
and in pregnancy and lactation.
Nutritional Requirements
Nutritional Research Council recommends daily intake
of 1.0 to 1.5 mg of thiamine for adults which is increased
with increased muscular activity, dietary carbohydrates
and in pregnancy and lactation.
15. Deficiency Manifestations
The deficiency of vitamin B1 results in a condition called
beriberi.
Deficiency of thiamine occurs in population who consume
exclusively polished rice as staple food.
The early symptoms of thiamine deficiency are anorexia
(lack of appetite) , nausea, mental confusion, peripheral
neuritis, and muscle fatigue.
Deficiency Manifestations
The deficiency of vitamin B1 results in a condition called
beriberi.
Deficiency of thiamine occurs in population who consume
exclusively polished rice as staple food.
The early symptoms of thiamine deficiency are anorexia
(lack of appetite) , nausea, mental confusion, peripheral
neuritis, and muscle fatigue.
16. Beriberi
Beriberi is divided into three types, relating to the body
system involved i.e. Nervous or cardiovascular or age of
patient (infantile).
1. Dry beriberi (neuritic beriberi): affects the nervous system
2. Wet beriberi (cardiac beriberi): affects cardiovascular system
3. Infantile beriberi: affects children of malnourished mothers.
Beriberi
Beriberi is divided into three types, relating to the body
system involved i.e. Nervous or cardiovascular or age of
patient (infantile).
1. Dry beriberi (neuritic beriberi): affects the nervous system
2. Wet beriberi (cardiac beriberi): affects cardiovascular system
3. Infantile beriberi: affects children of malnourished mothers.
17. Dry beriberi (neuritic beriberi)
It develops when the diet chronically contains slightly less
than requirements. It is characterized by:
–Vomiting.
–Poor appetite
–Peripheral neuritis
–Difficulty in walking
–Tingling or loss of sensation, numbness in hands
and feet
Dry beriberi (neuritic beriberi)
It develops when the diet chronically contains slightly less
than requirements. It is characterized by:
–Vomiting.
–Poor appetite
–Peripheral neuritis
–Difficulty in walking
–Tingling or loss of sensation, numbness in hands
and feet
19. Wet beriberi (cardiac beriberi)
It develops when the deficiency is more severe in which
cardiovascular system is affected in addition to
neurological symptoms.
Wet beriberi is characterized by:
− Peripheral Edema (swelling of lower legs)
−Heart enlargement and cardiac insuffi- ciency.
−Increased heart rate tachycardia
−It is sometimes fatal
Wet beriberi (cardiac beriberi)
It develops when the deficiency is more severe in which
cardiovascular system is affected in addition to
neurological symptoms.
Wet beriberi is characterized by:
− Peripheral Edema (swelling of lower legs)
−Heart enlargement and cardiac insuffi- ciency.
−Increased heart rate tachycardia
−It is sometimes fatal
20. Infantile beriberi
Infantile beriberi is observed in breast fed infants
(between two and six months of age) whose
mothers have inadequate thiamine intake. The
breast milk of these mothers is deficient in
thiamine.
Infantile beriberi
Infantile beriberi is observed in breast fed infants
(between two and six months of age) whose
mothers have inadequate thiamine intake. The
breast milk of these mothers is deficient in
thiamine.
21. It is characterized by
−GI disturbances such as vomiting ,diarrhea
− Cardiac dilation (enlargement of heart),
−Tachycardia (rapid heart rate)
− Convulsions,
−Edema
−In acute condition, the infant may die due to
cardiac failure.
It is characterized by
−GI disturbances such as vomiting ,diarrhea
− Cardiac dilation (enlargement of heart),
−Tachycardia (rapid heart rate)
− Convulsions,
−Edema
−In acute condition, the infant may die due to
cardiac failure.
22. Wernicke-Korsakoff Syndrome
Wernicke-Korsakoff Syndrome (WKS) is a neurological
disorder caused by a deficiency of vitamin thiamine
(vitamin B1) due to chronic alcohol consumption
It is also known as cerebral beriberi.
In chronic alcoholics, the nutritional deficiencies result
from either poor intake of food or malabsorp- tion of
nutrients from intestine.
Wernicke-Korsakoff Syndrome
Wernicke-Korsakoff Syndrome (WKS) is a neurological
disorder caused by a deficiency of vitamin thiamine
(vitamin B1) due to chronic alcohol consumption
It is also known as cerebral beriberi.
In chronic alcoholics, the nutritional deficiencies result
from either poor intake of food or malabsorp- tion of
nutrients from intestine.
23. Symptoms
Mental confusion and impaired short-term memory.
Impaired person’s ability to learn new information or tasks.
Ataxia (Loss of muscle coordination that can cause weakness
in limbs and leg tremor)
Paralysis of eye muscles
Nystagmus (Abnormal eye movements back & forth
movements of eye)
Double vision, eyelid drooping
Symptoms
Mental confusion and impaired short-term memory.
Impaired person’s ability to learn new information or tasks.
Ataxia (Loss of muscle coordination that can cause weakness
in limbs and leg tremor)
Paralysis of eye muscles
Nystagmus (Abnormal eye movements back & forth
movements of eye)
Double vision, eyelid drooping
24. Antimetabolites
Thiamine can be destroyed if the diet contains thiaminase.
Thiaminase is present in raw fish and seafood.
Thiamine Assay
Whole blood or Erythrocyte transketolase (requiring TPP
as a coenzyme) activity is used as a measure of thiamine
deficiency.
Antimetabolites
Thiamine can be destroyed if the diet contains thiaminase.
Thiaminase is present in raw fish and seafood.
Thiamine Assay
Whole blood or Erythrocyte transketolase (requiring TPP
as a coenzyme) activity is used as a measure of thiamine
deficiency.
25. Riboflavin (Vitamin B2)
Riboflavin is a yellow compound (Flavus = yellow in
Latin) consisting of a isoalloxazine ring with a ribitol
(sugar alcohol) side chain
26. Active Form of Riboflavin
Flavin mononucleotide (FMN)
Flavin adenine dinucleotide (FAD)
Active Form of Riboflavin
Flavin mononucleotide (FMN)
Flavin adenine dinucleotide (FAD)
28. Sources
The main dietary sources of riboflavin are yeast,
germinating seeds, green leafy vegetables milk and milk
products, eggs, liver , meat etc.
Cereals are a poor source
Sources
The main dietary sources of riboflavin are yeast,
germinating seeds, green leafy vegetables milk and milk
products, eggs, liver , meat etc.
Cereals are a poor source
29. Nutritional Requirements
The RDA for vitamin B2 is 1.3 to 1.7 mg for adults.
It is related to protein use and increases during growth,
pregnancy, lactation and wound healing.
Nutritional Requirements
The RDA for vitamin B2 is 1.3 to 1.7 mg for adults.
It is related to protein use and increases during growth,
pregnancy, lactation and wound healing.
30. Functions
Riboflavin is a precursor of coenzymes FMN and FAD, which
are required by several oxidation-reduction reactions in
metabolism.
FMN and FAD serve as coenzymes for oxidoreductase
enzymes involved in carbohydrate, protein, lipid, nucleic acid
metabolism and electron transport chain.
Decarboxylation of pyruvate and α-ketoglutarate requires FAD
Fatty acyl CoA dehydrogenase requires FAD in fatty acid
oxidation
Functions
Riboflavin is a precursor of coenzymes FMN and FAD, which
are required by several oxidation-reduction reactions in
metabolism.
FMN and FAD serve as coenzymes for oxidoreductase
enzymes involved in carbohydrate, protein, lipid, nucleic acid
metabolism and electron transport chain.
Decarboxylation of pyruvate and α-ketoglutarate requires FAD
Fatty acyl CoA dehydrogenase requires FAD in fatty acid
oxidation
31. Synthesis of active form of folate (5-methyl THF) requires
FADH2
FAD is required to convert tryptophan to niacin (vit B3)
Reduction of the oxidized form of glutathione (GSSG) to
its reduced form (GSH) is also FAD dependent. Thus they
are also involved in detoxification reactions
It is needed for maintenance of mucosal epithelial &
ocular tissues.
Synthesis of active form of folate (5-methyl THF) requires
FADH2
FAD is required to convert tryptophan to niacin (vit B3)
Reduction of the oxidized form of glutathione (GSSG) to
its reduced form (GSH) is also FAD dependent. Thus they
are also involved in detoxification reactions
It is needed for maintenance of mucosal epithelial &
ocular tissues.
32. Deficiency Manifestations
Riboflavin deficiency (ariboflavinosis) is quite
rare. It is most commonly seen in chronic
alcoholics.
Deficiency Manifestations
Riboflavin deficiency (ariboflavinosis) is quite
rare. It is most commonly seen in chronic
alcoholics.
33. The characteristic symptoms of riboflavin deficiency are:
Cheilosis: Cracks at the angles of the mouth,
Glossitis: Inflammation of the tongue that becomes
swollen and magenta colored
Dermatitis: Rough and scaly skin
Vascularization (the development of blood vessels)
of cornea. The eyes become red, itchy, watery and
sensitive to bright light.
The characteristic symptoms of riboflavin deficiency are:
Cheilosis: Cracks at the angles of the mouth,
Glossitis: Inflammation of the tongue that becomes
swollen and magenta colored
Dermatitis: Rough and scaly skin
Vascularization (the development of blood vessels)
of cornea. The eyes become red, itchy, watery and
sensitive to bright light.
34. Niacin (Vitamin B3)
Structure
Niacin is a general name for the nicotinic acid and
nicotinamide, either of which may act as a source of the
vitamin in the diet. Niacin is a simple derivative of
pyridine.
Niacin (Vitamin B3)
Structure
Niacin is a general name for the nicotinic acid and
nicotinamide, either of which may act as a source of the
vitamin in the diet. Niacin is a simple derivative of
pyridine.
35. Active Form
Active forms of niacin are:
Nicotinamide adenine dinucleotide (NAD+)
Nicotinamide adenine dinucleotide phosphate (NADP+)
Active Form
Active forms of niacin are:
Nicotinamide adenine dinucleotide (NAD+)
Nicotinamide adenine dinucleotide phosphate (NADP+)
36.
37.
38. Sources
Yeast, liver, legumes and meats are major sources of niacin.
Limited quantities of niacin can also be obtained from the
metabolism of tryptophan. For every 60 mg of tryptophan, 1
mg equivalent of niacin can be generated.
Nutritional Requirement
The RDA for niacin is 15 to 20 mg.
Tryptophan can only provide 10% of the total niacin
requirement.
Sources
Yeast, liver, legumes and meats are major sources of niacin.
Limited quantities of niacin can also be obtained from the
metabolism of tryptophan. For every 60 mg of tryptophan, 1
mg equivalent of niacin can be generated.
Nutritional Requirement
The RDA for niacin is 15 to 20 mg.
Tryptophan can only provide 10% of the total niacin
requirement.
39. Functions
Niacin is a precursor of coenzymes, nicotinamide adenine
dinucleotide (NAD+) and nicotinamide adenine
dinucleotide phosphate (NADP+).
NAD+ and NADP+ are involved in various oxidation and
reduction reactions.
They are, therefore involved in many metabolic pathways
of carbohydrate, lipid and protein.
Functions
Niacin is a precursor of coenzymes, nicotinamide adenine
dinucleotide (NAD+) and nicotinamide adenine
dinucleotide phosphate (NADP+).
NAD+ and NADP+ are involved in various oxidation and
reduction reactions.
They are, therefore involved in many metabolic pathways
of carbohydrate, lipid and protein.
40. Generally, NAD+ catalyze oxidation-reduction reactions
in oxidative path- ways
, e.g. citric acid cycle and
glycolysis.
Whereas NADP+ are often found in pathways concerned
with reductive synthesis, e.g. synthesis of cholesterol,
fatty acid and pentose phosphate pathways.
Generally, NAD+ catalyze oxidation-reduction reactions
in oxidative path- ways
, e.g. citric acid cycle and
glycolysis.
Whereas NADP+ are often found in pathways concerned
with reductive synthesis, e.g. synthesis of cholesterol,
fatty acid and pentose phosphate pathways.
41.
42. Deficiency Manifestation
Pellagra
Deficiency of niacin in human causes pellagra, a
disease involving :
Skin
Gastrointestinal tract
Central nervous system.
Deficiency Manifestation
Pellagra
Deficiency of niacin in human causes pellagra, a
disease involving :
Skin
Gastrointestinal tract
Central nervous system.
43. The symptoms of pellagra are characterized by three ‘Ds’:
1. Photosensitive Dermatitis
2. Diarrhea
3. Depressive psychosis (dementia) and if not treated death.
Untreated pellagra is fatal.
The symptoms of pellagra are characterized by three ‘Ds’:
1. Photosensitive Dermatitis
2. Diarrhea
3. Depressive psychosis (dementia) and if not treated death.
Untreated pellagra is fatal.
44. Niacin deficiency occurs in:
Population dependent on maize (corn) or sorghum
(jowar) as the staple food.
In maize, niacin is present in bound form niacytin.
Sorghum content high amount of leucine. Excess of
leucine inhibit conversion of tryptophan to niacin
Niacin deficiency occurs in:
Population dependent on maize (corn) or sorghum
(jowar) as the staple food.
In maize, niacin is present in bound form niacytin.
Sorghum content high amount of leucine. Excess of
leucine inhibit conversion of tryptophan to niacin
45. Deficiency of vitamin B6 (pyridoxal phosphate) leads to
niacin deficiency as it is involved as a coenzyme in the
pathway of synthesis of niacin from tryptophan.
Malignant carcinoid syndrome in which tryptophan is
diverted to formation of serotonin.
In Hartnup disease, a genetic disorder in which tryptophan
absorption and trans- portation is impaired.
Deficiency of vitamin B6 (pyridoxal phosphate) leads to
niacin deficiency as it is involved as a coenzyme in the
pathway of synthesis of niacin from tryptophan.
Malignant carcinoid syndrome in which tryptophan is
diverted to formation of serotonin.
In Hartnup disease, a genetic disorder in which tryptophan
absorption and trans- portation is impaired.
47. Pantothenic Acid (Vitamin B5)
The name pantothenic acid is derived from the Greek word
‘pantothene,’meaning from “everywhere” and gives an
indication of the wide distribution of the vitamin in foods.
48. Structure
Pantothenic acid is formed by combination of
pantoic acid and β-alanine
Structure
Pantothenic acid is formed by combination of
pantoic acid and β-alanine
Structure of pantothenic acid.
49. Active form
1. Coenzyme-A (CoA-SH)
2. Acyl carrier protein (ACP).
Source
Eggs, liver, yeast, wheat germs, cereals, etc. are impor- tant
sources of pantothenic acid, although the vitamin is widely
distributed.
Active form
1. Coenzyme-A (CoA-SH)
2. Acyl carrier protein (ACP).
Source
Eggs, liver, yeast, wheat germs, cereals, etc. are impor- tant
sources of pantothenic acid, although the vitamin is widely
distributed.
50. Nutritional Requirement
The RDA of pantothenic acid is not well established. A
daily intake of about 5–10 mg is advised for adults
51. Functions
Pantothenic acid is a component of coenzyme-A (CoA-
SH) and acyl carrier protein (ACP).
The thiol (-SH) group of CoA-SH and ACP acts as a
carrier of acyl groups.
Coenzyme-A participates in reactions concerned with:
– Reactions of citric acid cycle
– Fatty acid synthesis and oxidation
– Synthesis of cholesterol
– Utilization of ketone bodies.
ACP participate in reactions concerned with fatty acid
synthesis.
Functions
Pantothenic acid is a component of coenzyme-A (CoA-
SH) and acyl carrier protein (ACP).
The thiol (-SH) group of CoA-SH and ACP acts as a
carrier of acyl groups.
Coenzyme-A participates in reactions concerned with:
– Reactions of citric acid cycle
– Fatty acid synthesis and oxidation
– Synthesis of cholesterol
– Utilization of ketone bodies.
ACP participate in reactions concerned with fatty acid
synthesis.
52. Deficiency Manifestations
No clear-cut case of pantothenic acid deficiency has been
reported.
Clinical signs observed in experimentally induced
deficiencies are:
Paraesthesia (abnormal tingling sensation)
Headache
Dizziness
Gastrointestinal malfunction.
Deficiency Manifestations
No clear-cut case of pantothenic acid deficiency has been
reported.
Clinical signs observed in experimentally induced
deficiencies are:
Paraesthesia (abnormal tingling sensation)
Headache
Dizziness
Gastrointestinal malfunction.
53. Pyridoxine (Vitamin B6)
Structure
Vitamin B6 consists of a mixture of three different closely
related pyridine derivatives namely:
1. Pyridoxine
2. Pyridoxal
3. Pyridoxamine.
All the three have equal vitamin activity, as they can be
interconverted in the body.
Pyridoxine (Vitamin B6)
Structure
Vitamin B6 consists of a mixture of three different closely
related pyridine derivatives namely:
1. Pyridoxine
2. Pyridoxal
3. Pyridoxamine.
All the three have equal vitamin activity, as they can be
interconverted in the body.
55. Active Form of Vitamin B6
Pyridoxal phosphate (PLP) is the active form of vitamin
B6.
56. Sources
Pyridoxine occurs mainly in plants, whereas pyridoxal
and pyridoxamine are present mainly in animal
products.
Major dietary sources of vitamin B6 are yeast,
unrefined cereals, pulses, meat, poultry fish, potatoes
and vegetables.
Dairy products and grains contribute lesser amounts.
Sources
Pyridoxine occurs mainly in plants, whereas pyridoxal
and pyridoxamine are present mainly in animal
products.
Major dietary sources of vitamin B6 are yeast,
unrefined cereals, pulses, meat, poultry fish, potatoes
and vegetables.
Dairy products and grains contribute lesser amounts.
57. Nutritional Requirement
The RDA for vitamin B6 is 1.6 to 2.0 mg.
Requirements increase during pregnancy and lactation
58. Functions
Active form of vitamin B6, pyridoxal phosphate (PLP)
acts as coenzyme in amino acid metabolism. For
example:
– Transamination
– Decarboxylation
– Nonoxidative deamination
– Trans-sulfuration
– Condensation reactions of amino acids.
Functions
Active form of vitamin B6, pyridoxal phosphate (PLP)
acts as coenzyme in amino acid metabolism. For
example:
– Transamination
– Decarboxylation
– Nonoxidative deamination
– Trans-sulfuration
– Condensation reactions of amino acids.
59. Transamination reactions
Transamination reactions are catalyzed by transaminases
and PLP acts as coenzyme converting amino acid to keto
acid, e.g. aspartate transaminase (AST) and alanine
transaminase (ALT)
Non-oxidative deamination
Hydroxyl group contain- ing amino acids (serine,
threonine) are non-oxidatively deaminated to α-keto acids
and ammonia, which requires PLP.
Transamination reactions
Transamination reactions are catalyzed by transaminases
and PLP acts as coenzyme converting amino acid to keto
acid, e.g. aspartate transaminase (AST) and alanine
transaminase (ALT)
Non-oxidative deamination
Hydroxyl group contain- ing amino acids (serine,
threonine) are non-oxidatively deaminated to α-keto acids
and ammonia, which requires PLP.
60. Decarboxylation reaction
PLP acts as coenzyme in decarboxylation of some amino
acids. The amino acids are decarboxylated to corresponding
amines.
– γ-Amino butyric acid (GABA)
– Serotonin and melatonin
– Histamine
– Catecholamines (dopamine, norepinephrine and
epinephrine)
Decarboxylation reaction
PLP acts as coenzyme in decarboxylation of some amino
acids. The amino acids are decarboxylated to corresponding
amines.
– γ-Amino butyric acid (GABA)
– Serotonin and melatonin
– Histamine
– Catecholamines (dopamine, norepinephrine and
epinephrine)
61. Trans- sulfuration reaction:
PLP is a coenzyme for cystathionine synthase involved in
synthesis of cysteine from methionine In these reactions
transfer of sulfur from methionine to serine occurs to
produce cysteine.
Condensation reactions
Pyridoxal phosphate is required for the condensation
reaction of L-glycine and succinyl CoA in the synthesis of
heme.
Trans- sulfuration reaction:
PLP is a coenzyme for cystathionine synthase involved in
synthesis of cysteine from methionine In these reactions
transfer of sulfur from methionine to serine occurs to
produce cysteine.
Condensation reactions
Pyridoxal phosphate is required for the condensation
reaction of L-glycine and succinyl CoA in the synthesis of
heme.
62. Other reactions requiring PLP are:
– For niacin coenzyme (NAD+/NADP+) synthesis
from tryptophan
– For synthesis of serine from glycine
– FOR the synthesis of sphingomyelin.
Other reactions requiring PLP are:
– For niacin coenzyme (NAD+/NADP+) synthesis
from tryptophan
– For synthesis of serine from glycine
– FOR the synthesis of sphingomyelin.
63. Deficiency Manifestations
Vitamin B6 deficiency causes neurological disorders such
as depression, nervousness and irritability.
Severe deficiency of pyridoxine causes epileptic seizures
(convulsions) in infants.
Demyelination of nerves causes peripheral neuro- pathy
.
Vitamin B6 deficiency causes hypochromic micro- cytic
anemia due to decreased heme synthesis.
Deficiency Manifestations
Vitamin B6 deficiency causes neurological disorders such
as depression, nervousness and irritability.
Severe deficiency of pyridoxine causes epileptic seizures
(convulsions) in infants.
Demyelination of nerves causes peripheral neuro- pathy
.
Vitamin B6 deficiency causes hypochromic micro- cytic
anemia due to decreased heme synthesis.
64. The commonest cause of pyridoxine deficiency is:
Drug antagonism, e.g. isoniazide (INH), used in the
treatment of tuberculosis and penicillamide used in the
treatment of Wilson’s disease and rheumatoid arthritis can
combine with pyridoxal phosphate forming an inactive
derivative with pyridoxal phosphate.
Alcoholism: Alcoholics may be deficient owing to
metabolism of ethanol to acetaldehyde, which stimulates
hydrolysis of the phosphate of the pyridoxal phosphate
The commonest cause of pyridoxine deficiency is:
Drug antagonism, e.g. isoniazide (INH), used in the
treatment of tuberculosis and penicillamide used in the
treatment of Wilson’s disease and rheumatoid arthritis can
combine with pyridoxal phosphate forming an inactive
derivative with pyridoxal phosphate.
Alcoholism: Alcoholics may be deficient owing to
metabolism of ethanol to acetaldehyde, which stimulates
hydrolysis of the phosphate of the pyridoxal phosphate
65. Biotin
Biotin was known formerly as vitamin H.
Structure
It consists of a tetrahydro-thiophene ring bound to an
imidazole ring and a valeric acid side chain.
Biotin
Biotin was known formerly as vitamin H.
Structure
It consists of a tetrahydro-thiophene ring bound to an
imidazole ring and a valeric acid side chain.
67. Sources
It is widely distributed in foods.
Liver, kidneys, vegetables and egg yolk are the
important sources of biotin.
Biotin is also synthesized by intestinal bacteria.
Sources
It is widely distributed in foods.
Liver, kidneys, vegetables and egg yolk are the
important sources of biotin.
Biotin is also synthesized by intestinal bacteria.
68. Active Form of Biotin
Enzyme-bound biotin, biocytin is an active form of biotin.
Biotin is covalently bound to ε- amino group of lysine of an
enzyme to form biocytin.
Nutritional Requirements
A daily intake of about 150–300 mg is recommended for
adults. Biotin is synthesized by intestinal micro- organisms in
such a large quantities that a dietary source is probably not
necessary.
Active Form of Biotin
Enzyme-bound biotin, biocytin is an active form of biotin.
Biotin is covalently bound to ε- amino group of lysine of an
enzyme to form biocytin.
Nutritional Requirements
A daily intake of about 150–300 mg is recommended for
adults. Biotin is synthesized by intestinal micro- organisms in
such a large quantities that a dietary source is probably not
necessary.
69. Functions
Biotin is a coenzyme of carboxylase reactions, where it is a
carrier of CO2.
Conversion of acetyl-CoA into malonyl-CoA catalyzed
by acetyl-CoA carboxylase in fatty acid synthesis.
Conversion of pyruvate into oxaloacetate, catalyzed by
pyruvate carboxylase in gluconeogenesis .
Functions
Biotin is a coenzyme of carboxylase reactions, where it is a
carrier of CO2.
Conversion of acetyl-CoA into malonyl-CoA catalyzed
by acetyl-CoA carboxylase in fatty acid synthesis.
Conversion of pyruvate into oxaloacetate, catalyzed by
pyruvate carboxylase in gluconeogenesis .
70. Conversion of propionyl-CoA to D-methyl malonyl-CoA
catalyzed by propionyl-CoA carboxylase in the pathway
of conversion of propionate to succinate.
Catabolism of branched chain amino acid catalyzed by β-
methylcrotonyl-CoA carboxylase
Conversion of propionyl-CoA to D-methyl malonyl-CoA
catalyzed by propionyl-CoA carboxylase in the pathway
of conversion of propionate to succinate.
Catabolism of branched chain amino acid catalyzed by β-
methylcrotonyl-CoA carboxylase
71. Biotin Independent Carboxylation Reaction
Formation of carbamoyl phosphate by carbamoyl
phosphate synthetase in urea cycle.
Addition of CO2 to form C6 in purine ring.
Conversion of pyruvate to malate by malic enzyme.
Biotin Independent Carboxylation Reaction
Formation of carbamoyl phosphate by carbamoyl
phosphate synthetase in urea cycle.
Addition of CO2 to form C6 in purine ring.
Conversion of pyruvate to malate by malic enzyme.
72. Deficiency Manifestation
Since biotin is widely distributed in plant and animal
foods and intestinal bacterial flora supply adequate
amounts of biotin, the natural deficiency of biotin is not
well characterized in humans.
The experimentally induced symptoms of biotin
deficiency are nausea, anorexia, glossitis, dermatitis,
alopecia (loss of hair), depression and muscular pain.
Deficiency Manifestation
Since biotin is widely distributed in plant and animal
foods and intestinal bacterial flora supply adequate
amounts of biotin, the natural deficiency of biotin is not
well characterized in humans.
The experimentally induced symptoms of biotin
deficiency are nausea, anorexia, glossitis, dermatitis,
alopecia (loss of hair), depression and muscular pain.
73.
74. Deficiency of biotin occurs in:
The people with the unusual dietary habit of consuming
large amounts of uncooked eggs. Egg white contains the
glycoprotein avidin, which binds the imidazole group of
biotin and prevents biotin absorption.
Use of antibiotics, that inhibit the growth of intestinal
bacteria, eliminates this source of biotin and leads to
deficiency of biotin.
Deficiency of biotin occurs in:
The people with the unusual dietary habit of consuming
large amounts of uncooked eggs. Egg white contains the
glycoprotein avidin, which binds the imidazole group of
biotin and prevents biotin absorption.
Use of antibiotics, that inhibit the growth of intestinal
bacteria, eliminates this source of biotin and leads to
deficiency of biotin.
75. Folic Acid
Structure
Folic acid consists of three components:
1. Pteridine ring,
2. P-amino benzoic acid (PABA) and
3. L-glutamic acid
In a folic acid molecule, the number of glutamic acid
residues varies from one to seven. Folic acid usually
has one glutamic acid residue.
Folic Acid
Structure
Folic acid consists of three components:
1. Pteridine ring,
2. P-amino benzoic acid (PABA) and
3. L-glutamic acid
In a folic acid molecule, the number of glutamic acid
residues varies from one to seven. Folic acid usually
has one glutamic acid residue.
77. Active Form of Folic Acid
Tetrahydrofolate (THF) is the active form of folic acid.
Source
Folic acid is found in green leafy vegetables, liver, yeast.
The word folate is related to folium which means leaf in
Latin.
Active Form of Folic Acid
Tetrahydrofolate (THF) is the active form of folic acid.
Source
Folic acid is found in green leafy vegetables, liver, yeast.
The word folate is related to folium which means leaf in
Latin.
82. Functions
Tetrahydrofolate (THF) acts as a carrier of one-
carbon units. The one carbon units are:
Methyl CH3
Methylene CH2
Methenyl CH
Formyl CHO
Formimino CH = NH
Functions
Tetrahydrofolate (THF) acts as a carrier of one-
carbon units. The one carbon units are:
Methyl CH3
Methylene CH2
Methenyl CH
Formyl CHO
Formimino CH = NH
83. One carbon unit binds to THF through N5 or N10 or both
N5, N10 position.
The THF coenzymes serve as acceptors or donors of one
carbon units in a variety of reactions involved in amino
acid and nucleic acid metabolism.
One carbon unit binds to THF through N5 or N10 or both
N5, N10 position.
The THF coenzymes serve as acceptors or donors of one
carbon units in a variety of reactions involved in amino
acid and nucleic acid metabolism.
84. Five major reactions in which THF is involved are:
1. Conversion of serine to glycine:
The conversion of serine to glycine is accompanied
by the formation of N5,N10- methylene THF.
2. Synthesis of thymidylate (pyrimidine nucleo- tide):
The enzyme thymidylate synthase that converts
deoxyuridylate (dUMP) into thymidy- late (TMP)
uses N5, N10- methylene THF as the methyl donor
for this reaction.
Five major reactions in which THF is involved are:
1. Conversion of serine to glycine:
The conversion of serine to glycine is accompanied
by the formation of N5,N10- methylene THF.
2. Synthesis of thymidylate (pyrimidine nucleo- tide):
The enzyme thymidylate synthase that converts
deoxyuridylate (dUMP) into thymidy- late (TMP)
uses N5, N10- methylene THF as the methyl donor
for this reaction.
85. 3. Catabolism of histidine :
Histidine in the course of its catabolism is converted into
formimino- glutamate(FIGLU). This molecule donate the
formimino group to THF to produce N 5 formimino THF.
4. Synthesis of purine:
N5-Formyl THF inter- mediate formedin histidine
catabolism is used in the biosyn- thesis of purineand
therefore in the formation of both DNA and RNA.
5. Synthesis of methionine from homocysteine:
Homocysteine is converted to methionine in presence of
N5-methyl THF, and vitamin B12.
3. Catabolism of histidine :
Histidine in the course of its catabolism is converted into
formimino- glutamate(FIGLU). This molecule donate the
formimino group to THF to produce N 5 formimino THF.
4. Synthesis of purine:
N5-Formyl THF inter- mediate formedin histidine
catabolism is used in the biosyn- thesis of purineand
therefore in the formation of both DNA and RNA.
5. Synthesis of methionine from homocysteine:
Homocysteine is converted to methionine in presence of
N5-methyl THF, and vitamin B12.
86. – In this reaction the methyl group bound to cobalamin
(Vitamin B12) is transferred to homocysteine to form
methionine and the cobalamin then removes the methyl
group from N5-methyl THF to form THF.
– This step is essential for the liberation of free THF and
for its repeated use in one carbon metabolism. In B12
deficiency, conversion of N5-methyl THF to free THF is
blocked.
– In this reaction the methyl group bound to cobalamin
(Vitamin B12) is transferred to homocysteine to form
methionine and the cobalamin then removes the methyl
group from N5-methyl THF to form THF.
– This step is essential for the liberation of free THF and
for its repeated use in one carbon metabolism. In B12
deficiency, conversion of N5-methyl THF to free THF is
blocked.
89. Deficiency Manifestations
Megaloblastic or macrocytic anemia
Accumulation and excretion of FIGLU in the urine
Hyperhomocysteinemia
Neural tube defect in foetus
Deficiency Manifestations
Megaloblastic or macrocytic anemia
Accumulation and excretion of FIGLU in the urine
Hyperhomocysteinemia
Neural tube defect in foetus
91. Cobalamin (Vitamin B12)
Structure
Vitamin B12 bears a complex corrin ring (containing
pyrrols similar to porphyrin), linked to a cobalt atom
held in the center of the corrin ring, by four coordination
bonds with the nitrogen of the pyrrole groups.
Cobalamin (Vitamin B12)
Structure
Vitamin B12 bears a complex corrin ring (containing
pyrrols similar to porphyrin), linked to a cobalt atom
held in the center of the corrin ring, by four coordination
bonds with the nitrogen of the pyrrole groups.
92. The remaining coordination bonds of the cobalt are
linked with the nitrogen of dimethylbenzimidazole
nucleotide and sixth bond is linked to either methyl or
5'-deoxy- adenosylor hydroxy group to form
methyl- cobalamin, adenosylcobalamin or
hydroxycobalamin respectively
The remaining coordination bonds of the cobalt are
linked with the nitrogen of dimethylbenzimidazole
nucleotide and sixth bond is linked to either methyl or
5'-deoxy- adenosylor hydroxy group to form
methyl- cobalamin, adenosylcobalamin or
hydroxycobalamin respectively
93.
94. Structure of Vit B12.
(R: either
methyl
or
deoxyadenosyl
or
hydroxy group)
Structure of Vit B12.
(R: either
methyl
or
deoxyadenosyl
or
hydroxy group)
95. Active form of Vitamin B12
Methylcobalamin
Deoxyadenosylcobalamin.
Sources
Dietary sources of vitamin B12 are of animal origin ;
meat, eggs, milk, dairy products, fish, poultry, etc.
Vitamin B12 is absent in plant foods.
Humans obtain small amounts of B12 from intestinal
flora.
Active form of Vitamin B12
Methylcobalamin
Deoxyadenosylcobalamin.
Sources
Dietary sources of vitamin B12 are of animal origin ;
meat, eggs, milk, dairy products, fish, poultry, etc.
Vitamin B12 is absent in plant foods.
Humans obtain small amounts of B12 from intestinal
flora.
96. Nutritional Requirements (RDA )
3 μg with higher allowances for pregnancy and
lactating women.
Nutritional Requirements (RDA )
3 μg with higher allowances for pregnancy and
lactating women.
98. • The intestinal absorption of vitamin B12 requires an
intrinsic factor (IF), a glycoprotein secreted by parietal
cells of the stomach.
• In stomach IF binds the dietary vitamin B12 to form
vitamin B12-IF complex.
• This complex binds to specific receptors on the surface of
the mucosal cells of the ileum.
• After binding to the receptor, the bound vitamin B12 is
released from the complex and enters the illeal mucosal
cells through a Ca2+
dependent process.
• The intestinal absorption of vitamin B12 requires an
intrinsic factor (IF), a glycoprotein secreted by parietal
cells of the stomach.
• In stomach IF binds the dietary vitamin B12 to form
vitamin B12-IF complex.
• This complex binds to specific receptors on the surface of
the mucosal cells of the ileum.
• After binding to the receptor, the bound vitamin B12 is
released from the complex and enters the illeal mucosal
cells through a Ca2+
dependent process.
99. Functions
There are only two human enzyme systems that are
known to require vitamin B12 coenzyme.
1. Isomerization of methylmalonyl-CoA to succinyl-CoA
2. Conversion of homocysteine to methionine
Functions
There are only two human enzyme systems that are
known to require vitamin B12 coenzyme.
1. Isomerization of methylmalonyl-CoA to succinyl-CoA
2. Conversion of homocysteine to methionine
100. Role of vit B12 in
isomerization of
methylmalonyl-CoA to
succinyl-CoA
101. Role of vit B12 conversion of homocysteine to methionine
This is the only mammalian reaction require both vitamins
103. Vitamin B12 Deficiency Causes
Functional Folate Deficiency: The Folate Trap
S-adenosyl methionine forms homocysteine, which may
be remethylated by methyltetrahydrofolate catalysed by
methionine synthase, a vitamin B12 dependent enzyme.
Impairment of methionine synthase in vitamin B12
deficiency results in the accumulation of
methyltetrahydrofolate that cannot be used and cannot be
converted to free THF.
Vitamin B12 Deficiency Causes
Functional Folate Deficiency: The Folate Trap
S-adenosyl methionine forms homocysteine, which may
be remethylated by methyltetrahydrofolate catalysed by
methionine synthase, a vitamin B12 dependent enzyme.
Impairment of methionine synthase in vitamin B12
deficiency results in the accumulation of
methyltetrahydrofolate that cannot be used and cannot be
converted to free THF.
104. Thus, most of THF is irreversibly “trapped” as methyl
THF.
There is therefore functional deficiency of folate,
secondary to the deficiency of vitamin B12.
Folate trap creates folate deficiency and an adequate
supply of free THF is not available for the synthesis of
purine and pyrimidine bases.
Thus, most of THF is irreversibly “trapped” as methyl
THF.
There is therefore functional deficiency of folate,
secondary to the deficiency of vitamin B12.
Folate trap creates folate deficiency and an adequate
supply of free THF is not available for the synthesis of
purine and pyrimidine bases.
105.
106. Vitamin C (Ascorbic Acid)
Structure
It is a six-carbon sugar derivative .
Humans cannot synthesize ascorbic acid, due to lack of
the enzyme gluconolactone oxidase.
Vitamin C (Ascorbic Acid)
Structure
It is a six-carbon sugar derivative .
Humans cannot synthesize ascorbic acid, due to lack of
the enzyme gluconolactone oxidase.
108. Active Form of Ascorbic Acid
Ascorbic acid itself is an active form.
Sources
The main dietary sources of vitamin C are leafy
vegetables and fruits, especially citrus fruits, strawberries,
tomatoes, spinach and potatoes.
Cereals contain no vitamin C.
Animal tissues and dairy products are very poor sources.
Active Form of Ascorbic Acid
Ascorbic acid itself is an active form.
Sources
The main dietary sources of vitamin C are leafy
vegetables and fruits, especially citrus fruits, strawberries,
tomatoes, spinach and potatoes.
Cereals contain no vitamin C.
Animal tissues and dairy products are very poor sources.
110. Functions
Vitamin C is the coenzyme for two groups of
hydroxylases.
–Copper containing hydroxylases
–α-ketoglutarate linked iron containing
hydroxylases
Ascorbic acid has specific roles in the number of non-
enzymatic effects as result of its action as a reducing
agent and oxygen radical quencher.
Functions
Vitamin C is the coenzyme for two groups of
hydroxylases.
–Copper containing hydroxylases
–α-ketoglutarate linked iron containing
hydroxylases
Ascorbic acid has specific roles in the number of non-
enzymatic effects as result of its action as a reducing
agent and oxygen radical quencher.
111. Role of Ascorbic acid in the copper containing hydroxylases
Dopamine β-hydroxylase is a copper containing enzyme
involved in the synthesis of the catecholamines
(norepinephrine and epinephrine), from tyrosine in the
adrenal medulla and central nervous system.
A number of peptide hormones have a carboxy terminal
amide that is derived from a terminal glycine residue. This
glycine is hydroxylated on the α-carbon by a copper
containing enzyme, peptidylglycine hydroxylase, which
again, requires ascorbate for reduction of Cu2+
.
Role of Ascorbic acid in the copper containing hydroxylases
Dopamine β-hydroxylase is a copper containing enzyme
involved in the synthesis of the catecholamines
(norepinephrine and epinephrine), from tyrosine in the
adrenal medulla and central nervous system.
A number of peptide hormones have a carboxy terminal
amide that is derived from a terminal glycine residue. This
glycine is hydroxylated on the α-carbon by a copper
containing enzyme, peptidylglycine hydroxylase, which
again, requires ascorbate for reduction of Cu2+
.
112. Role of Ascorbic acid in the iron containing hydroxylases
Proline hydroxylases and lysine hydroxylases are required for the
postsynthetic modification of procollagen to collagen.
Aspartate β-hydroxylase is required for the postsynthetic
modification of the precursor of protein C.
Vitamin K-dependent protease that hydrolyses activated factor V
in the blood clotting cascade.
Trimethyllysine and γ-butyrobetain hydroxylases are required for
the synthesis of carnitine.
Role of Ascorbic acid in the iron containing hydroxylases
Proline hydroxylases and lysine hydroxylases are required for the
postsynthetic modification of procollagen to collagen.
Aspartate β-hydroxylase is required for the postsynthetic
modification of the precursor of protein C.
Vitamin K-dependent protease that hydrolyses activated factor V
in the blood clotting cascade.
Trimethyllysine and γ-butyrobetain hydroxylases are required for
the synthesis of carnitine.
113. Non-enzymatic effects as result of its action as a reducing
agent and oxygen radical quencher
Ascorbic acid is a water soluble antioxidant:
– It reduces oxidized vitamin E (tocopherol) to
regenerate functional vitamin E.
– Vitamin C thought to be involved in the prevention of
atherosclerosis and coronary heart disease by
preventing oxidation of LDL.
Non-enzymatic effects as result of its action as a reducing
agent and oxygen radical quencher
Ascorbic acid is a water soluble antioxidant:
– It reduces oxidized vitamin E (tocopherol) to
regenerate functional vitamin E.
– Vitamin C thought to be involved in the prevention of
atherosclerosis and coronary heart disease by
preventing oxidation of LDL.
114. – Antioxidant property of vitamin C is also associated
with prevention of cancer by inhibiting nitrosamine
formation from naturally occurring nitrates during
digestion.
• In addition to other roles of vitamin C, it enhances the
absorption of inorganic iron. Ascorbic acid facilitates the
absorption of iron from intestine by reducing it to the
Fe++ (ferrous) state.
– Antioxidant property of vitamin C is also associated
with prevention of cancer by inhibiting nitrosamine
formation from naturally occurring nitrates during
digestion.
• In addition to other roles of vitamin C, it enhances the
absorption of inorganic iron. Ascorbic acid facilitates the
absorption of iron from intestine by reducing it to the
Fe++ (ferrous) state.
115. Deficiency Manifestation
Deficiency has been observed in infants receiving un-
supplemented cow’s milk and in infants receiving breast
milk from deficient mother.
Deficiency occurs most commonly in the elderly,
especially those who do not eat fresh fruits and vegetables
and who tend to cook in frying pans, the combination of
heat and large area of food in contact with air irreversibly
oxidizes the vitamin and loses its biological activity.
Deficiency also can occur in iron overload.
Deficiency Manifestation
Deficiency has been observed in infants receiving un-
supplemented cow’s milk and in infants receiving breast
milk from deficient mother.
Deficiency occurs most commonly in the elderly,
especially those who do not eat fresh fruits and vegetables
and who tend to cook in frying pans, the combination of
heat and large area of food in contact with air irreversibly
oxidizes the vitamin and loses its biological activity.
Deficiency also can occur in iron overload.
116. Scurvy
Deficiency of ascorbic acid causes scurvy.
Vitamin C is required for formation of collagen, where it is
needed for the hydroxylation of proline and lysine residues, of
protocollagen.
Hydroxyproline and hydroxylysine are essential for the
collagen cross-linking and collagen strength and stability.
Since vitamin C is required for normal collagen formation,
vitamin C is also involved in bone and dentin formation as well
as wound healing process.
Scurvy
Deficiency of ascorbic acid causes scurvy.
Vitamin C is required for formation of collagen, where it is
needed for the hydroxylation of proline and lysine residues, of
protocollagen.
Hydroxyproline and hydroxylysine are essential for the
collagen cross-linking and collagen strength and stability.
Since vitamin C is required for normal collagen formation,
vitamin C is also involved in bone and dentin formation as well
as wound healing process.
117. Symptoms of scurvy
Symptoms of scurvy are related to deficient collagen
formation. These include:
– Fragility of vascular walls causing bleeding tendency,
muscle weakness, soft spongy, swollen bleeding
gums, loosening of teeth.
– Abnormal bone development and osteoporosis. In
children bone formation is impaired.
Symptoms of scurvy
Symptoms of scurvy are related to deficient collagen
formation. These include:
– Fragility of vascular walls causing bleeding tendency,
muscle weakness, soft spongy, swollen bleeding
gums, loosening of teeth.
– Abnormal bone development and osteoporosis. In
children bone formation is impaired.
118. – Poor wound healing.
– Anemia due to impaired erythropoiesis.
– Milder forms of vitamin C deficiency are more
common and manifestation of such include easy
bruising (contusion) and formation of petechiae both
due to increased capillary fragility.
– Poor wound healing.
– Anemia due to impaired erythropoiesis.
– Milder forms of vitamin C deficiency are more
common and manifestation of such include easy
bruising (contusion) and formation of petechiae both
due to increased capillary fragility.
119. Vitamin A
Structure
Vitamin A contains a single 6-membered ring to which is
attached an 11-carbon side chain.
Vitamin A is an alcohol (retinol), but can be converted
into an aldehyde (retinal), or acid (retinoic acid).
Vitamin A
Structure
Vitamin A contains a single 6-membered ring to which is
attached an 11-carbon side chain.
Vitamin A is an alcohol (retinol), but can be converted
into an aldehyde (retinal), or acid (retinoic acid).
121. Active Form
Vitamin A consists of three biologically active molecules
which are collectively known as retinoids.
1. Retinol: Primary alcohol (CH2OH) containing form
2. Retinal: Aldehyde (CHO) containing form
3. Retinoic acid: Carboxyl (COOH) containing form
Active Form
Vitamin A consists of three biologically active molecules
which are collectively known as retinoids.
1. Retinol: Primary alcohol (CH2OH) containing form
2. Retinal: Aldehyde (CHO) containing form
3. Retinoic acid: Carboxyl (COOH) containing form
122. Each of these compounds are derived from the plant precursor
molecule, β-carotene.
β-carotene which consists of two molecules of retinal linked
at their aldehyde ends is also referred to as the provitamin
form of vitamin A.
The retinol and retinal are interconverted by enzyme retinal
aldehyde reductase.
The retinoic acid is formed by oxidation of retinal. The
retinoic acid can not be reduced to either retinol or retinal
Each of these compounds are derived from the plant precursor
molecule, β-carotene.
β-carotene which consists of two molecules of retinal linked
at their aldehyde ends is also referred to as the provitamin
form of vitamin A.
The retinol and retinal are interconverted by enzyme retinal
aldehyde reductase.
The retinoic acid is formed by oxidation of retinal. The
retinoic acid can not be reduced to either retinol or retinal
124. Sources
The richest dietary sources are fish liver oils (cod liver
oil). Meat is rather low in vitamin A.
Other good sources are milk and dairy products, dark-
green leaves, such as spinach and yellow and red fruits
and vegetables, such as carrots, tomatoes, and peaches
etc.
Sources
The richest dietary sources are fish liver oils (cod liver
oil). Meat is rather low in vitamin A.
Other good sources are milk and dairy products, dark-
green leaves, such as spinach and yellow and red fruits
and vegetables, such as carrots, tomatoes, and peaches
etc.
125. Nutritional Requirements
The RDA of vitamin A for adults is 800–1000 retinol
equivalents. (1 retinol equivalent = 1 mg retinol = 6 mg β-
carotene).
Nutritional Requirements
The RDA of vitamin A for adults is 800–1000 retinol
equivalents. (1 retinol equivalent = 1 mg retinol = 6 mg β-
carotene).
126. Functions of Vitamin A
Vitamin A is required for a variety of functions such as
– Vision
– Cell differentiation and growth
– Mucus secretion
– Maintenance of epithelial cells
Functions of Vitamin A
Vitamin A is required for a variety of functions such as
– Vision
– Cell differentiation and growth
– Mucus secretion
– Maintenance of epithelial cells
127. Different forms of the vitamin have different functions.
– Retinal and retinol are involved in vision.
– Retinoic acid is involved in cellular differentiation
and metabolic processes.
– β-carotene is involved in antioxidant function.
Different forms of the vitamin have different functions.
– Retinal and retinol are involved in vision.
– Retinoic acid is involved in cellular differentiation
and metabolic processes.
– β-carotene is involved in antioxidant function.
128. Role of Vitamin A in Vision
The role of vitamin A in vision has been known through
the studies of G Wald, who received the Nobel Prize in
1943
The cyclic events occur in the process of vision, known
as rhodopsin cycle or Wald’s visual cycle
Role of Vitamin A in Vision
The role of vitamin A in vision has been known through
the studies of G Wald, who received the Nobel Prize in
1943
The cyclic events occur in the process of vision, known
as rhodopsin cycle or Wald’s visual cycle
129. Both rod and cone cells of retina contain a photoreceptor
pigment in their membrane and vitamin A is a component
of these pigments.
Rhodopsin or visual purple, the visual pigment of rod
cells in the retina consists of 11-cis-retinal bound to
protein opsin.
Both rod and cone cells of retina contain a photoreceptor
pigment in their membrane and vitamin A is a component
of these pigments.
Rhodopsin or visual purple, the visual pigment of rod
cells in the retina consists of 11-cis-retinal bound to
protein opsin.
131. When rhodopsin absorbs light, the 11-cis-retinal is
converted to all-trans retinal.
The isomerization is associated with a conforma- tional
change in the protein opsin.
Conformational changes in opsin generates a nerve
impulse that is trans- mitted by the optic nerve to the brain
.
This is followed by dissociation of the all-trans retinal
from opsin
When rhodopsin absorbs light, the 11-cis-retinal is
converted to all-trans retinal.
The isomerization is associated with a conforma- tional
change in the protein opsin.
Conformational changes in opsin generates a nerve
impulse that is trans- mitted by the optic nerve to the brain
.
This is followed by dissociation of the all-trans retinal
from opsin
132. The all-trans retinal is immediately isomerized by retinal
isomerase to 11-cis-retinal.
This combines with opsin to regenerate rhodopsin and
complete the visual cycle.
The conversion of all-trans retinal to 11-cis-retinal is
incomplete and therefore remaining all-trans retinal
which is not converted to 11-cis-retinal is converted to all-
trans retinol by alcohol dehydrogenase and is stored in the
liver.
The all-trans retinal is immediately isomerized by retinal
isomerase to 11-cis-retinal.
This combines with opsin to regenerate rhodopsin and
complete the visual cycle.
The conversion of all-trans retinal to 11-cis-retinal is
incomplete and therefore remaining all-trans retinal
which is not converted to 11-cis-retinal is converted to all-
trans retinol by alcohol dehydrogenase and is stored in the
liver.
133. When needed, retinol re-enters the circulation and is taken
up by the retina, where it is converted back to 11-cis-
retinal which combines with opsin again to form
rhodopsin
When needed, retinol re-enters the circulation and is taken
up by the retina, where it is converted back to 11-cis-
retinal which combines with opsin again to form
rhodopsin
134. Dark adaptation time
The time taken for regeneration of rhodopsin is known as
dark adaptation time. Dark adaptation time is increased in
vitamin A deficient individuals
135. Role of Vitamin A in Color Vision
Color vision is mediated by three pigments called
porphyropsin, iodopsin and cyanopsin and are sensitive to
the three essential colours: red, green and blue
respectively.
All these pigments consist of 11-cis-retinal bound to
protein opsin .
When light strikes retina, it bleaches one or more of these
pigments, depending on the color quality of the light.
The pigments are converted to all-trans retinal, and the
protein moiety opsin is released as in the case of
rhodopsin.
Role of Vitamin A in Color Vision
Color vision is mediated by three pigments called
porphyropsin, iodopsin and cyanopsin and are sensitive to
the three essential colours: red, green and blue
respectively.
All these pigments consist of 11-cis-retinal bound to
protein opsin .
When light strikes retina, it bleaches one or more of these
pigments, depending on the color quality of the light.
The pigments are converted to all-trans retinal, and the
protein moiety opsin is released as in the case of
rhodopsin.
136. This reaction gives rise to the nerve impulse that is read
out in the brain as color:
– Red if porphyropsin is split
– Green if iodopsin is split
– Blue if cyanopsin is split.
If mixtures of the three are converted, the color read out
in the brain depends on the proportions of the three split.
This reaction gives rise to the nerve impulse that is read
out in the brain as color:
– Red if porphyropsin is split
– Green if iodopsin is split
– Blue if cyanopsin is split.
If mixtures of the three are converted, the color read out
in the brain depends on the proportions of the three split.
137. Cellular Differentiation and Metabolic Effect
Retinoic acid is an important regulator of gene
expression especially during growth and development.
Retinoic acid is essential for normal gene expression
during embryonic development such as cell
differentiation in spermatogenesis and in the
differentiation of epithelial cells.
Cellular Differentiation and Metabolic Effect
Retinoic acid is an important regulator of gene
expression especially during growth and development.
Retinoic acid is essential for normal gene expression
during embryonic development such as cell
differentiation in spermatogenesis and in the
differentiation of epithelial cells.
138. Retinoic acids exert a number of metabolic effects on tissues.
These include:
–Control of biosynthesis of membrane glycoproteins
and glycosaminoglycans (mucopolysaccharide)
necessary for mucus secretion. The normal mucus
secretion maintains the epithelial surface moist and
prevents keratinization of epithelial cell.
–Control of biosynthesis of cholesterol.
Retinoic acids exert a number of metabolic effects on tissues.
These include:
–Control of biosynthesis of membrane glycoproteins
and glycosaminoglycans (mucopolysaccharide)
necessary for mucus secretion. The normal mucus
secretion maintains the epithelial surface moist and
prevents keratinization of epithelial cell.
–Control of biosynthesis of cholesterol.
139. Antioxidant Function
β-carotene is an antioxidant and may play a role in
trapping free radicals in tissues.
The antioxidant property of lipid soluble vitamin A may
account for its possible anticancer activity.
High levels of dietary carotenoids have been associated
with a decreased risk of cardiovascular disease
Antioxidant Function
β-carotene is an antioxidant and may play a role in
trapping free radicals in tissues.
The antioxidant property of lipid soluble vitamin A may
account for its possible anticancer activity.
High levels of dietary carotenoids have been associated
with a decreased risk of cardiovascular disease
140. Deficiency Manifestation
Clinically, degenerative changes in eyes and skin are
observed commonly in individuals with vitamin A
deficiency.
Vitamin deficiency may be primary (dietary
insufficiency) or secondary.
Deficiency Manifestation
Clinically, degenerative changes in eyes and skin are
observed commonly in individuals with vitamin A
deficiency.
Vitamin deficiency may be primary (dietary
insufficiency) or secondary.
141. The causes of secondary deficiency may include:
– Impaired absorption of lipids
– Failure to synthesize apo B-48 and therefore inability
to form chylomicrons into which vitamin A is
normally incorporated after absorption.
– Lack of lipase, as in pancreatitis.
– Failure in converting β - carotene to retinol; because
of an enzyme defect.
The causes of secondary deficiency may include:
– Impaired absorption of lipids
– Failure to synthesize apo B-48 and therefore inability
to form chylomicrons into which vitamin A is
normally incorporated after absorption.
– Lack of lipase, as in pancreatitis.
– Failure in converting β - carotene to retinol; because
of an enzyme defect.
142. – Impaired storage in hepatic cell in liver disease.
– Failure to synthesize retinol binding proteins, thus
affecting transport to target tissues.
143. Effect on Vision
The earliest symptoms of vitamin A deficiency is:
– Impaired dark adaptation or night blindness
(nyctalopia)
– Poor vision in dim light
– Xerophthalmia.
Effect on Vision
The earliest symptoms of vitamin A deficiency is:
– Impaired dark adaptation or night blindness
(nyctalopia)
– Poor vision in dim light
– Xerophthalmia.
144. Night blindness (nyctalopia)
This is characterized by loss of vision in night (in dim or
poor light) since dark adaptation time is increased.
Prolonged deficiency of vitamin A leads to an irreversible
loss of visual cells.
Severe vitamin A deficiency causes dryness of cornea and
conjunctiva, a clinical condition termed as xerophthalmia
(dry eyes).
Night blindness (nyctalopia)
This is characterized by loss of vision in night (in dim or
poor light) since dark adaptation time is increased.
Prolonged deficiency of vitamin A leads to an irreversible
loss of visual cells.
Severe vitamin A deficiency causes dryness of cornea and
conjunctiva, a clinical condition termed as xerophthalmia
(dry eyes).
145.
146. If this situation prolongs, keratinization and ulceration of
cornea takes place
This results in destruction of cornea. The cornea becomes
totally opaque resulting in permanent loss of vision
(blindness), a clinical condition termed as keratomalacia.
White opaque spots develop on either side of cornea in
vitamin A deficiency are known as Bitot’s spot.
If this situation prolongs, keratinization and ulceration of
cornea takes place
This results in destruction of cornea. The cornea becomes
totally opaque resulting in permanent loss of vision
(blindness), a clinical condition termed as keratomalacia.
White opaque spots develop on either side of cornea in
vitamin A deficiency are known as Bitot’s spot.
147.
148. Effect on Skin and Epithelial Cells
Vitamin A deficiency causes keratinization of epithelial
cells of skin which leads to keratosis of hair follicles,
and dry, rough and scaly skin.
Keratinization of epithelial cells of respiratory, urinary
tract makes them susceptible to infections.
Effect on Skin and Epithelial Cells
Vitamin A deficiency causes keratinization of epithelial
cells of skin which leads to keratosis of hair follicles,
and dry, rough and scaly skin.
Keratinization of epithelial cells of respiratory, urinary
tract makes them susceptible to infections.
149. Other Symptoms of Vitamin A Deficiency
Failure of growth in children.
Faulty bone modelling producing thick cancellous
(spongy) bones instead of thinner and more compact ones.
Abnormalities of reproduction, including degeneration of
the testes, abortion or the production of malformed
offspring.
Other Symptoms of Vitamin A Deficiency
Failure of growth in children.
Faulty bone modelling producing thick cancellous
(spongy) bones instead of thinner and more compact ones.
Abnormalities of reproduction, including degeneration of
the testes, abortion or the production of malformed
offspring.
150. Hypervitaminosis A
Excessive intakes of vitamin A lead to accumulation beyond the
capacity of intracellular binding proteins. Unbound vitamin A
causes membrane lysis and tissue damage. Symptoms of toxicity
affect:
The central nervous system and leads to headache, nausea,
ataxia, and anorexia. These all associated with increased
cerebrospinal fluid pressure.
The liver: hepatomegaly with histological changes and
hyperlipidemia
Hypervitaminosis A
Excessive intakes of vitamin A lead to accumulation beyond the
capacity of intracellular binding proteins. Unbound vitamin A
causes membrane lysis and tissue damage. Symptoms of toxicity
affect:
The central nervous system and leads to headache, nausea,
ataxia, and anorexia. These all associated with increased
cerebrospinal fluid pressure.
The liver: hepatomegaly with histological changes and
hyperlipidemia
151. Calcium homeostasis: thickening of the long bones,
hypercalcemia, and calcification of soft tissues, bone and
joint pain,
The skin: loss of hair (alopecia), scaly and rough skin.
In pregnant women, the hypervitaminosis A may cause
congenital malformation in growing fetus (teratogenic
effect).
Calcium homeostasis: thickening of the long bones,
hypercalcemia, and calcification of soft tissues, bone and
joint pain,
The skin: loss of hair (alopecia), scaly and rough skin.
In pregnant women, the hypervitaminosis A may cause
congenital malformation in growing fetus (teratogenic
effect).
152. Why Vitamin A is Considered as a Hormone?
Within cells both retinol and retinoic acid function by binding
to specific receptor proteins present in the nucleus of target
tissues.
Following binding, the receptor-vitamin complex interacts
with several genes involved in growth and differentiation and
affects expression of these genes.
Why Vitamin A is Considered as a Hormone?
Within cells both retinol and retinoic acid function by binding
to specific receptor proteins present in the nucleus of target
tissues.
Following binding, the receptor-vitamin complex interacts
with several genes involved in growth and differentiation and
affects expression of these genes.
153. Vitamin D (Cholecalciferol)
Vitamin D is also known as calciferol because of its role
in calcium metabolism and antirachitic factor because it
prevents rickets.
Vitamin D (Cholecalciferol)
Vitamin D is also known as calciferol because of its role
in calcium metabolism and antirachitic factor because it
prevents rickets.
154. Vitamin D could be thought of as a hormone
rather than a vitamin
As it can be synthesized in the body
It is released in the circulation
Has distinct target organs
Action of vitamin D is similar to steroid hormones. It
binds to a receptor in the cytosol. Following binding, the
receptor vitamin complex interacts with DNA to
stimulate the synthesis of calcium binding protein.
Vitamin D could be thought of as a hormone
rather than a vitamin
As it can be synthesized in the body
It is released in the circulation
Has distinct target organs
Action of vitamin D is similar to steroid hormones. It
binds to a receptor in the cytosol. Following binding, the
receptor vitamin complex interacts with DNA to
stimulate the synthesis of calcium binding protein.
155. Structure
Vitamin D is a steroid compound. The naturally produced
vitamin D3 or cholecalciferol is obtained from animal
sources in the diet, or made in the skin by the action of
ultraviolet light from sunlight on
Structure
Vitamin D is a steroid compound. The naturally produced
vitamin D3 or cholecalciferol is obtained from animal
sources in the diet, or made in the skin by the action of
ultraviolet light from sunlight on
157. The formation of vitamin D3 in the body and
vitamin D2 commercially.
158. Active Form of Vitamin
Cholecalciferol is an inactive form of vitamin D.
It needs further metabolism to produce the active form of
the vitamin. 1, 25 dihydroxycholecalciferol also known
as calcitriol is the active form of vitamin D.
Active Form of Vitamin
Cholecalciferol is an inactive form of vitamin D.
It needs further metabolism to produce the active form of
the vitamin. 1, 25 dihydroxycholecalciferol also known
as calcitriol is the active form of vitamin D.
160. Sources
Best sources are cod liver oil and often fish oils and
sunlight induced synthesis of vitamin D3 in skin.
Egg yolk and liver are good sources.
Nutritional Requirement
The daily requirements of vitamin D is 200–400 IU.
Sources
Best sources are cod liver oil and often fish oils and
sunlight induced synthesis of vitamin D3 in skin.
Egg yolk and liver are good sources.
Nutritional Requirement
The daily requirements of vitamin D is 200–400 IU.
161. Functions
Vitamin D (Calcitriol) plays an essential role as a
hormone in the regulation of calcium and phosphorus
metabolism.
It maintains the normal plasma level of calcium and
phosphorus by acting on intestine, kidneys and bones.
Functions
Vitamin D (Calcitriol) plays an essential role as a
hormone in the regulation of calcium and phosphorus
metabolism.
It maintains the normal plasma level of calcium and
phosphorus by acting on intestine, kidneys and bones.
162. Action of calcitriol on intestine
It increases the plasma calcium and phosphorus
concentration by stimulating the absorption of
calcium and phosphorus from the intestine.
Action of calcitriol on kidney
It stimulates the reabsorption of calcium and
phosphorus from the kidney and decreases their
excretion.
Action of calcitriol on intestine
It increases the plasma calcium and phosphorus
concentration by stimulating the absorption of
calcium and phosphorus from the intestine.
Action of calcitriol on kidney
It stimulates the reabsorption of calcium and
phosphorus from the kidney and decreases their
excretion.
163. Action of calcitriol on bone
– Calcitriol promotes the mineralization of bones by
deposition of calcium and phosphorus.
– Calcitriol along with PTH stimulates the mobilization
of calcium and phosphorus from bone.
Action of calcitriol on bone
– Calcitriol promotes the mineralization of bones by
deposition of calcium and phosphorus.
– Calcitriol along with PTH stimulates the mobilization
of calcium and phosphorus from bone.
164. Sites of formation of vitamin D3 to its metabolically
active form 1,25-dihydroxychole- calciferol and its
function.
1,25-DHCC: 1,25-dihydroxycholecalciferol;
PTH: parathyroid hormone
Sites of formation of vitamin D3 to its metabolically
active form 1,25-dihydroxychole- calciferol and its
function.
1,25-DHCC: 1,25-dihydroxycholecalciferol;
PTH: parathyroid hormone
168. Rickets
Rickets is characterized by formation of soft and pliable
bones due to poor mineralization and calcium deficiency.
Due to softness, the weight bearing bones are bent and
deformed.
The main features of the rickets are, a large head with
protruding forehead, pigeon chest, bow legs, (curved
legs), knock knees and abnormal curvature of the spine
(kyphosis).
Rickets
Rickets is characterized by formation of soft and pliable
bones due to poor mineralization and calcium deficiency.
Due to softness, the weight bearing bones are bent and
deformed.
The main features of the rickets are, a large head with
protruding forehead, pigeon chest, bow legs, (curved
legs), knock knees and abnormal curvature of the spine
(kyphosis).
170. Rachitic children are usually anemic or prone to
infections. Rickets can be fatal when severe.
Rickets is characterized by low plasma levels of calcium
and phosphorus and high alkaline phosphatase activity.
Rachitic children are usually anemic or prone to
infections. Rickets can be fatal when severe.
Rickets is characterized by low plasma levels of calcium
and phosphorus and high alkaline phosphatase activity.
171. Osteomalacia (Adult Rickets)
Deficiency of vitamin D in adults causes osteomalacia.
This is a condition similar to that of rickets.
Osteomalacia characterized by demineralization of
previously formed bones, Demineralization of bones
makes them soft and susceptible to fractures.
Osteomalacia especially occurs in women who have little
exposure to sunlight, and especially after several
pregnancies
Osteomalacia (Adult Rickets)
Deficiency of vitamin D in adults causes osteomalacia.
This is a condition similar to that of rickets.
Osteomalacia characterized by demineralization of
previously formed bones, Demineralization of bones
makes them soft and susceptible to fractures.
Osteomalacia especially occurs in women who have little
exposure to sunlight, and especially after several
pregnancies
172. Renal Rickets (Renal Osteodystrophy)
In chronic renal failure synthesis of calcitriol in kidney is
impaired. As a result, the deficiency of calcitriol occurs
which leads to hypocalcemia and hyperphosphatemia.
It can be treated by oral or intravenous administration of
calcitriol (active form of vitamin D).
Renal Rickets (Renal Osteodystrophy)
In chronic renal failure synthesis of calcitriol in kidney is
impaired. As a result, the deficiency of calcitriol occurs
which leads to hypocalcemia and hyperphosphatemia.
It can be treated by oral or intravenous administration of
calcitriol (active form of vitamin D).
173. Vitamin D Resistant Rickets
As the name implies, this is a disease which does not
respond to treatment with vitamin D.
There are various possible causes of this condition and
all involve a defect in the metabolism or mechanism of
action of 1,25 dihydroxycholecalciferol.
Vitamin D Resistant Rickets
As the name implies, this is a disease which does not
respond to treatment with vitamin D.
There are various possible causes of this condition and
all involve a defect in the metabolism or mechanism of
action of 1,25 dihydroxycholecalciferol.
174. – Due to defective vitamin D receptor
– Due to a defective 1, α-hydroxylase activity in kidney
– Due to liver disease and kidney failure as the
production of 25-hydroxycholecalciferol and 1,25
dihydroxycholecalciferol respectively will be
inefficient in the damaged tissue
– Due to defective vitamin D receptor
– Due to a defective 1, α-hydroxylase activity in kidney
– Due to liver disease and kidney failure as the
production of 25-hydroxycholecalciferol and 1,25
dihydroxycholecalciferol respectively will be
inefficient in the damaged tissue
175. Hypervitaminosis D
High doses of vitamin D over a long period are toxic.
The early symptoms of hypervitaminosis D include nausea,
vomiting, anorexia, increased thirst, loss of weight, etc.
Hypercalcemia is seen due to increased bone resorption and
intestinal absorption of calcium.
The prolonged hypercalcemia causes calcification of soft
tissues and organs such as kidney and may lead to formation
of stones in the kidneys.
Hypervitaminosis D
High doses of vitamin D over a long period are toxic.
The early symptoms of hypervitaminosis D include nausea,
vomiting, anorexia, increased thirst, loss of weight, etc.
Hypercalcemia is seen due to increased bone resorption and
intestinal absorption of calcium.
The prolonged hypercalcemia causes calcification of soft
tissues and organs such as kidney and may lead to formation
of stones in the kidneys.
177. Sources
The major dietary sources of vitamin E are fats and oils.
The richest sources are germ oil, corn oil, fish oil, eggs,
lettuce and alfalfa.
Nutritional Requirements
A daily consumption of about:
10 mg (15 IU) of α-tocopherol for a man
8 mg (12 IU) for α- woman is recommended.
One mg of α-tocopherol is equal to 1.5 IU.
Sources
The major dietary sources of vitamin E are fats and oils.
The richest sources are germ oil, corn oil, fish oil, eggs,
lettuce and alfalfa.
Nutritional Requirements
A daily consumption of about:
10 mg (15 IU) of α-tocopherol for a man
8 mg (12 IU) for α- woman is recommended.
One mg of α-tocopherol is equal to 1.5 IU.
178. Functions
Vitamin E acts as a natural antioxidant by scavenging
free radicals and molecular oxygen.
Vitamin E is important for preventing peroxidation of
polyunsaturated fatty acids in cell membranes.
Protection of erythrocyte membrane from oxidant is the
major role of vitamin E in humans. It protects the RBCs
from hemolysis.
Functions
Vitamin E acts as a natural antioxidant by scavenging
free radicals and molecular oxygen.
Vitamin E is important for preventing peroxidation of
polyunsaturated fatty acids in cell membranes.
Protection of erythrocyte membrane from oxidant is the
major role of vitamin E in humans. It protects the RBCs
from hemolysis.
179. Vitamin E also helps to prevent oxidation of LDL.
Oxidized LDL may be more atherogenic than native LDL
and thus vitamin E may protect against athreo- matous
coronary heart disease.
Whether vitamin E affects human fertility is unknown.
In animals, vitamin E is required for normal reproduction
and prevents sterility.
Vitamin E also helps to prevent oxidation of LDL.
Oxidized LDL may be more atherogenic than native LDL
and thus vitamin E may protect against athreo- matous
coronary heart disease.
Whether vitamin E affects human fertility is unknown.
In animals, vitamin E is required for normal reproduction
and prevents sterility.
180. Deficiency Manifestation
The major symptom of vitamin E deficiency in human is
hemolytic anemia due to an increased red blood cell fragility.
Another symptom of vitamin E deficiency is retrolental
fibroplasia (RLF) observed in some premature infants of low
birth weight. Children with this defect show neuropathy.
Hypervitaminosis E
Unlike other fat soluble vitamins such as A and D, vitamin E
does not seem to have toxic effects.
Deficiency Manifestation
The major symptom of vitamin E deficiency in human is
hemolytic anemia due to an increased red blood cell fragility.
Another symptom of vitamin E deficiency is retrolental
fibroplasia (RLF) observed in some premature infants of low
birth weight. Children with this defect show neuropathy.
Hypervitaminosis E
Unlike other fat soluble vitamins such as A and D, vitamin E
does not seem to have toxic effects.
181. Vitamin K
This vitamin is called an anti-hemorrhagic factor as its
deficiency produced uncontrolled hemorrhages due to
defect in blood coagulation.
In 1929, H Dam gave the name koagulation vitamin from
the Danish word koagulation. It is now called vitamin K.
Vitamin K
This vitamin is called an anti-hemorrhagic factor as its
deficiency produced uncontrolled hemorrhages due to
defect in blood coagulation.
In 1929, H Dam gave the name koagulation vitamin from
the Danish word koagulation. It is now called vitamin K.
182. Structure
Vitamin K1 or phylloquinone derived from plant.
Vitamin K2 or menaquinones, produced by
microorganisms.
Vitamin K3 or menadione is a synthetic product
Structure
Vitamin K1 or phylloquinone derived from plant.
Vitamin K2 or menaquinones, produced by
microorganisms.
Vitamin K3 or menadione is a synthetic product
184. Sources
Excellent sources are cabbage, cauliflower, spinach and
other green vegetables.
Good sources include tomatoes, cheese, dairy products,
meat, egg yolk, etc.
The vitamin is also synthesized by microorganisms in the
intestinal tract.
Nutritional Requirements
The suggested intake for adults is 70–140 mg/day.
Sources
Excellent sources are cabbage, cauliflower, spinach and
other green vegetables.
Good sources include tomatoes, cheese, dairy products,
meat, egg yolk, etc.
The vitamin is also synthesized by microorganisms in the
intestinal tract.
Nutritional Requirements
The suggested intake for adults is 70–140 mg/day.
185. Functions of Vitamin K
Vitamin K plays an important role in blood coagulation.
Vitamin K is required for the activation of blood clotting
factors, prothrombin (II), factor VII, IX and X.
These blood clotting proteins are synthesized in liver in
inactive form, and are converted to active form by
vitamin K dependent carboxylation reaction.
In this, vitamin K dependent carboxylase enzyme adds
the extra carboxyl group at -carbon of glutamic acid
residues of inactive blood clotting factors.
Functions of Vitamin K
Vitamin K plays an important role in blood coagulation.
Vitamin K is required for the activation of blood clotting
factors, prothrombin (II), factor VII, IX and X.
These blood clotting proteins are synthesized in liver in
inactive form, and are converted to active form by
vitamin K dependent carboxylation reaction.
In this, vitamin K dependent carboxylase enzyme adds
the extra carboxyl group at -carbon of glutamic acid
residues of inactive blood clotting factors.
186. Role of vitamin K in the gamma-carboxylation of glutamyl residues of inactive
proteins of blood-clotting factors.
187. Vitamin K is also required for the carboxylation of
glutamic acid residues of osteocalcin, a Ca2+ binding
protein present in bone.
Anticoagulants, Dicumarol and warfarin are structurally
similar to vitamin K and inhibit the action of vitamin K.
Vitamin K is also required for the carboxylation of
glutamic acid residues of osteocalcin, a Ca2+ binding
protein present in bone.
Anticoagulants, Dicumarol and warfarin are structurally
similar to vitamin K and inhibit the action of vitamin K.
188. Deficiency Manifestation
Vitamin K is widely distributed in nature and its production
by the intestinal micro flora ensures that dietary deficiency
does not occur.
Vitamin K deficiency is associated with hemorrhagic
disease.
In vitamin K deficiency, clotting time of blood is
increased. Uncontrolled hemorrhages occur on minor
injuries as a result of reduction in prothrombin and other
clotting factors.
Deficiency Manifestation
Vitamin K is widely distributed in nature and its production
by the intestinal micro flora ensures that dietary deficiency
does not occur.
Vitamin K deficiency is associated with hemorrhagic
disease.
In vitamin K deficiency, clotting time of blood is
increased. Uncontrolled hemorrhages occur on minor
injuries as a result of reduction in prothrombin and other
clotting factors.
189. Vitamin K deficiency, however, is found in:
Patients with liver disease and biliary obstruction. Biliary
obstruction inhibits the entry of bile salts to the intestine.
In new-born infants, because the placenta does not pass
the vitamin to the fetus efficiently, and the gut is sterile
immediately after birth.
Following antibiotic therapy that sterilizes the gut.
In fat malabsorption, that impairs absorption of vitamin
K.
Vitamin K deficiency, however, is found in:
Patients with liver disease and biliary obstruction. Biliary
obstruction inhibits the entry of bile salts to the intestine.
In new-born infants, because the placenta does not pass
the vitamin to the fetus efficiently, and the gut is sterile
immediately after birth.
Following antibiotic therapy that sterilizes the gut.
In fat malabsorption, that impairs absorption of vitamin
K.
190. Hypervitaminosis K
Excessive doses of vitamin K produce a hemolytic anemia
(due to increased breakdown of RBCs) and jaundice (in
infants).
Hypervitaminosis K
Excessive doses of vitamin K produce a hemolytic anemia
(due to increased breakdown of RBCs) and jaundice (in
infants).