This document discusses vitamin D deficiency (rickets) in children. It covers the sources and mechanisms of vitamin D, causes of rickets including nutritional deficiencies and genetic disorders, clinical features, investigations, and management. The key points are:
- Vitamin D is important for intestinal calcium absorption and bone mineralization. Deficiency can cause the bone disease rickets in children.
- Rickets is usually caused by nutritional vitamin D deficiency in breastfed infants without supplements. It can also be caused by genetic disorders that impair vitamin D metabolism.
- Clinical features include bone deformities, muscle weakness, fractures, and in severe cases, hypocalcemia. Radiographs show characteristic changes in the growth plates of long
Este documento resume la estructura química, fuentes, absorción, requerimientos diarios recomendados, funciones, deficiencia y toxicidad de la vitamina B6. Explica que la vitamina B6 existe en tres formas principales que son hidrolizadas en el intestino y absorbidas en el yeyuno. Además, destaca que la vitamina B6 es necesaria para mantener la homeostasis de enzimas y producir energía en los animales domésticos.
This document discusses the role of calcium and vitamin D in reducing fracture risk. It notes that osteoporotic fractures are increasing with aging and are associated with morbidity, disability, and mortality. Adequate calcium and vitamin D intake helps maximize bone mineral density and prevents falls. The document reviews clinical trials on calcium and vitamin D supplementation for fracture prevention and concludes that daily supplementation of 800 IU of vitamin D and 1000 mg of calcium can effectively reduce fracture risk, especially in institutionalized elderly individuals. Compliance with long-term supplementation is important to maintain benefits.
Free radicals are highly reactive molecules that can cause damage to biomolecules, cells, and tissues. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are examples of free radicals and other molecules that are not free radicals but can generate free radicals. Free radicals can harm proteins, lipids, carbohydrates, and nucleic acids but also have some beneficial effects. Antioxidants help prevent or limit the damage caused by free radicals by preventing oxidation reactions. Antioxidants include enzymes like superoxide dismutase and glutathione peroxidase as well as nutrients like carotenoids, ascorbic acid, and α-tocopherols.
This document discusses vitamin D deficiency (rickets) in children. It covers the sources and mechanisms of vitamin D, causes of rickets including nutritional deficiencies and genetic disorders, clinical features, investigations, and management. The key points are:
- Vitamin D is important for intestinal calcium absorption and bone mineralization. Deficiency can cause the bone disease rickets in children.
- Rickets is usually caused by nutritional vitamin D deficiency in breastfed infants without supplements. It can also be caused by genetic disorders that impair vitamin D metabolism.
- Clinical features include bone deformities, muscle weakness, fractures, and in severe cases, hypocalcemia. Radiographs show characteristic changes in the growth plates of long
Este documento resume la estructura química, fuentes, absorción, requerimientos diarios recomendados, funciones, deficiencia y toxicidad de la vitamina B6. Explica que la vitamina B6 existe en tres formas principales que son hidrolizadas en el intestino y absorbidas en el yeyuno. Además, destaca que la vitamina B6 es necesaria para mantener la homeostasis de enzimas y producir energía en los animales domésticos.
This document discusses the role of calcium and vitamin D in reducing fracture risk. It notes that osteoporotic fractures are increasing with aging and are associated with morbidity, disability, and mortality. Adequate calcium and vitamin D intake helps maximize bone mineral density and prevents falls. The document reviews clinical trials on calcium and vitamin D supplementation for fracture prevention and concludes that daily supplementation of 800 IU of vitamin D and 1000 mg of calcium can effectively reduce fracture risk, especially in institutionalized elderly individuals. Compliance with long-term supplementation is important to maintain benefits.
Free radicals are highly reactive molecules that can cause damage to biomolecules, cells, and tissues. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are examples of free radicals and other molecules that are not free radicals but can generate free radicals. Free radicals can harm proteins, lipids, carbohydrates, and nucleic acids but also have some beneficial effects. Antioxidants help prevent or limit the damage caused by free radicals by preventing oxidation reactions. Antioxidants include enzymes like superoxide dismutase and glutathione peroxidase as well as nutrients like carotenoids, ascorbic acid, and α-tocopherols.
This document discusses the role of antioxidants in health and disease. It defines free radicals and describes how they are produced endogenously through metabolism and exogenously through environmental factors. Free radicals can cause oxidative damage but are balanced by the body's antioxidant defense system, which includes antioxidant enzymes like catalase and glutathione peroxidase, chain breaking antioxidants like vitamin E and beta-carotene, and transition metal binding proteins. The document outlines the sources and roles of various reactive oxygen species and antioxidants in the body.
Definition of Rickets &Osteomalacia.
Etiology of Rickets & Osteomalacia
Rickets :
is defective mineralization of bones before epiphyseal closure (at growth plate) due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium ,potentially leading to fractures and deformity.
Osteomalacia :
is a similar condition occurring in adults, generally due to impaired mineralization of the bone matrix. Due to a deficiency of vitamin D.
Etiology:
Vit D deficiency :
low intake plus inadequate sunlight exposure
malabsorption
Abnormal Vit D metabolism:
Impaired 25 OH Vitamin D production (Liver diseases)
Impaired 1,25 OH2 Vitamin D production (chronic renal failure or vitamin D-resistant rickets type I ).
Vitamin D receptor defects (vitaminD-resistant rickets type II)
Low calcium intake
Hypophosphatemia :
Low intake.
Inherited or acquired defects in renal tubular phosphate reabsorption.
Tumors that secrete phosphaturic substance.
Rickets and Osteomalacia are impaired memorization of the bone.
Causes of Rickets and Osteomalacia :
Vit D deficiency
Low calcium intake
Abnormal Vit D metabolism
Hypophosphatemia
This document summarizes water soluble vitamins, focusing on vitamin C. It discusses the chemistry, biosynthesis, metabolism, functions, deficiency, sources and recommended intake of vitamin C. Vitamin C is a water soluble vitamin that acts as a coenzyme in several enzymatic reactions. It is essential for collagen formation, iron absorption and immune function. Deficiency results in scurvy, characterized by bleeding gums and fragile blood vessels. Good dietary sources include citrus fruits and vegetables.
Este documento describe las vitaminas y minerales más importantes, sus fuentes principales, y los efectos de la deficiencia. Explica que las vitaminas y minerales son nutrientes esenciales para el buen funcionamiento del organismo y la prevención de enfermedades. Además, destaca la importancia de incluir estos nutrientes en la dieta diaria a pesar de las dificultades actuales para obtener una alimentación saludable.
Vitamina B9 SNP del 5MTHFR, metilazione e iperomocisteinemiaMaurizio Salamone
I folati non sono tutti uguali. Polimorfismi genetici limitatnti possono portare a bassi valori di folati attivi circolanti con implicazioni negative sui processi di metilazione e sul metabolismo dell'omocisteina. La conseguenza più comune di una carenza di folati è l'iperomocisteinemia, ma si possono avere anche deficit nella produzione delle basi del DNA. aumento dei processi di aging e disturbi in altri importanti processi metabolici. Il 5 metil tetraidrofolato è una soluzione semplice e poco costosa per rimediare efficacemente.
All About Vitamin D
Follow me on SlideShare ,Follow on blogger.com and linkedIn...
https://www.slideshare.net/YashLodha11/vitamin-d-247723886/edit?src=slideview
https://www.linkedin.com/in/yash-lodha-047728211/
https://www.blogger.com/blog/posts/2577104637130363155
This presentation introduces a brief and rapid review for an important research area (oxidative stress) and its relation to liver fibrosis.
Liver fibrosis is very important for us as we are facing a very dangerous and continuously growing problem in Egypt, HEPATIC PATIENTS COMPLICATIONS.
Vitamin D is a fat-soluble vitamin derived from cholesterol that functions as a steroid hormone. It is present in the skin in an inactive form, 7-dehydrocholesterol, and is converted to the active form calciferol when the skin is exposed to sunlight. The active form of vitamin D binds to vitamin D receptors in target cells and acts as a transcription factor that modulates gene expression involved in calcium absorption and bone health. Risk factors for vitamin D deficiency include inadequate sun exposure, skin pigmentation, obesity, and certain medical conditions or medications. Vitamin D deficiency can lead to rickets in children and osteomalacia in adults, and has also been associated with increased risk of diabetes, preecl
Vitamin B2, also known as riboflavin, is an essential component of coenzymes involved in redox reactions in the body. It acts as a precursor to FMN and FAD, which are cofactors for redox enzymes. Deficiency can result from poor intake, malabsorption, drug interactions, and genetic defects affecting flavin metabolism. Symptoms include sore throat, cheilosis, and glossitis. Status is assessed by urinary riboflavin levels, erythrocyte glutathione reductase activity, and direct measurement of flavins in plasma and erythrocytes.
Iperomocisteinemia e L-Metilfolato in Neurologia: trattamento, dosaggi, tempiGabriele Carbone
Omocisteina come fattore di rischio di malattie cerebrali su base vascolare e neurodegenerativa (Alzheimer, Demenze Vascolari, Sclerosi mulktipla, polineuropatie ecc.)
Este documento presenta un índice de un proyecto de investigación sobre el ácido fólico. El índice incluye secciones como planteamiento del problema, justificación, objetivo, metodología, hipótesis, marco histórico y marco teórico. El objetivo general es dar a conocer qué es el ácido fólico, sus beneficios y las consecuencias de su falta.
The document discusses antioxidants and their role in human health. It defines antioxidants as molecules that inhibit the oxidation of other molecules and prevent free radical damage. Free radicals are unstable molecules that can damage cells, but antioxidant enzymes work to stabilize free radicals. Many health conditions are linked to oxidative stress caused by free radicals, including aging, cancer, diabetes and neurodegenerative diseases. The body has both endogenous and dietary antioxidant systems to protect against free radical damage through catalytic removal of radicals and protection of macromolecules.
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Vitamins are essential organic substances needed by the body in small amounts to perform specific metabolic functions. There are 13 legitimate vitamins that exist as either fat-soluble (A, D, E, K) or water-soluble (C, B-complex). Fat-soluble vitamins are stored in tissues while water-soluble vitamins are not stored and require consistent dietary intake. Deficiencies of vitamins can result in diseases like rickets, osteomalacia, beriberi, and pellagra depending on the specific vitamin lacking in the diet.
Riboflavin,flavoproteins and their clinical applicationsrohini sane
A presentation in lucid-style on Riboflavin (vitamin B2), Flavoproteins and their clinical applications for MBBS , BDS , B Pham and Biotechnology students to facilitate easy leaning.
Vitamin D is an essential vitamin that must be metabolized to become biologically active. It plays an important role in calcium homeostasis, bone and muscle health, immune function, and the regulation of cell growth. The best indicator of vitamin D status is the measurement of 25-hydroxyvitamin D in the blood, as it reflects vitamin D from dietary intake and sunlight exposure. Low vitamin D levels have been associated with increased risk of various chronic diseases. Vitamin D deficiency can lead to impaired bone mineralization and increased fracture risk.
Vitamin D has widespread effects beyond bone health. It acts as a pleiotropic hormone that regulates over 200 genes and has important immunomodulatory properties. Maintaining optimal vitamin D levels may help reduce the risk of infections like tuberculosis and exacerbations of COPD, as well as cancers, cardiovascular disease, fractures and autoimmune disorders. More research is still needed but achieving a serum 25(OH)D level of at least 30 ng/mL through supplementation appears to provide the most benefits.
Vitamin D deficiency is common worldwide and can cause many health issues. It is involved in calcium absorption and bone health. Deficiency leads to osteomalacia and rickets in children, and increases risk of fractures in adults. It may also play roles in cardiovascular disease, diabetes, cancer prevention, autoimmune disease, pregnancy complications, muscle weakness, and mortality. Treatment involves dietary sources of vitamin D, supplementation, and sunlight exposure.
This document discusses the role of antioxidants in health and disease. It defines free radicals and describes how they are produced endogenously through metabolism and exogenously through environmental factors. Free radicals can cause oxidative damage but are balanced by the body's antioxidant defense system, which includes antioxidant enzymes like catalase and glutathione peroxidase, chain breaking antioxidants like vitamin E and beta-carotene, and transition metal binding proteins. The document outlines the sources and roles of various reactive oxygen species and antioxidants in the body.
Definition of Rickets &Osteomalacia.
Etiology of Rickets & Osteomalacia
Rickets :
is defective mineralization of bones before epiphyseal closure (at growth plate) due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium ,potentially leading to fractures and deformity.
Osteomalacia :
is a similar condition occurring in adults, generally due to impaired mineralization of the bone matrix. Due to a deficiency of vitamin D.
Etiology:
Vit D deficiency :
low intake plus inadequate sunlight exposure
malabsorption
Abnormal Vit D metabolism:
Impaired 25 OH Vitamin D production (Liver diseases)
Impaired 1,25 OH2 Vitamin D production (chronic renal failure or vitamin D-resistant rickets type I ).
Vitamin D receptor defects (vitaminD-resistant rickets type II)
Low calcium intake
Hypophosphatemia :
Low intake.
Inherited or acquired defects in renal tubular phosphate reabsorption.
Tumors that secrete phosphaturic substance.
Rickets and Osteomalacia are impaired memorization of the bone.
Causes of Rickets and Osteomalacia :
Vit D deficiency
Low calcium intake
Abnormal Vit D metabolism
Hypophosphatemia
This document summarizes water soluble vitamins, focusing on vitamin C. It discusses the chemistry, biosynthesis, metabolism, functions, deficiency, sources and recommended intake of vitamin C. Vitamin C is a water soluble vitamin that acts as a coenzyme in several enzymatic reactions. It is essential for collagen formation, iron absorption and immune function. Deficiency results in scurvy, characterized by bleeding gums and fragile blood vessels. Good dietary sources include citrus fruits and vegetables.
Este documento describe las vitaminas y minerales más importantes, sus fuentes principales, y los efectos de la deficiencia. Explica que las vitaminas y minerales son nutrientes esenciales para el buen funcionamiento del organismo y la prevención de enfermedades. Además, destaca la importancia de incluir estos nutrientes en la dieta diaria a pesar de las dificultades actuales para obtener una alimentación saludable.
Vitamina B9 SNP del 5MTHFR, metilazione e iperomocisteinemiaMaurizio Salamone
I folati non sono tutti uguali. Polimorfismi genetici limitatnti possono portare a bassi valori di folati attivi circolanti con implicazioni negative sui processi di metilazione e sul metabolismo dell'omocisteina. La conseguenza più comune di una carenza di folati è l'iperomocisteinemia, ma si possono avere anche deficit nella produzione delle basi del DNA. aumento dei processi di aging e disturbi in altri importanti processi metabolici. Il 5 metil tetraidrofolato è una soluzione semplice e poco costosa per rimediare efficacemente.
All About Vitamin D
Follow me on SlideShare ,Follow on blogger.com and linkedIn...
https://www.slideshare.net/YashLodha11/vitamin-d-247723886/edit?src=slideview
https://www.linkedin.com/in/yash-lodha-047728211/
https://www.blogger.com/blog/posts/2577104637130363155
This presentation introduces a brief and rapid review for an important research area (oxidative stress) and its relation to liver fibrosis.
Liver fibrosis is very important for us as we are facing a very dangerous and continuously growing problem in Egypt, HEPATIC PATIENTS COMPLICATIONS.
Vitamin D is a fat-soluble vitamin derived from cholesterol that functions as a steroid hormone. It is present in the skin in an inactive form, 7-dehydrocholesterol, and is converted to the active form calciferol when the skin is exposed to sunlight. The active form of vitamin D binds to vitamin D receptors in target cells and acts as a transcription factor that modulates gene expression involved in calcium absorption and bone health. Risk factors for vitamin D deficiency include inadequate sun exposure, skin pigmentation, obesity, and certain medical conditions or medications. Vitamin D deficiency can lead to rickets in children and osteomalacia in adults, and has also been associated with increased risk of diabetes, preecl
Vitamin B2, also known as riboflavin, is an essential component of coenzymes involved in redox reactions in the body. It acts as a precursor to FMN and FAD, which are cofactors for redox enzymes. Deficiency can result from poor intake, malabsorption, drug interactions, and genetic defects affecting flavin metabolism. Symptoms include sore throat, cheilosis, and glossitis. Status is assessed by urinary riboflavin levels, erythrocyte glutathione reductase activity, and direct measurement of flavins in plasma and erythrocytes.
Iperomocisteinemia e L-Metilfolato in Neurologia: trattamento, dosaggi, tempiGabriele Carbone
Omocisteina come fattore di rischio di malattie cerebrali su base vascolare e neurodegenerativa (Alzheimer, Demenze Vascolari, Sclerosi mulktipla, polineuropatie ecc.)
Este documento presenta un índice de un proyecto de investigación sobre el ácido fólico. El índice incluye secciones como planteamiento del problema, justificación, objetivo, metodología, hipótesis, marco histórico y marco teórico. El objetivo general es dar a conocer qué es el ácido fólico, sus beneficios y las consecuencias de su falta.
The document discusses antioxidants and their role in human health. It defines antioxidants as molecules that inhibit the oxidation of other molecules and prevent free radical damage. Free radicals are unstable molecules that can damage cells, but antioxidant enzymes work to stabilize free radicals. Many health conditions are linked to oxidative stress caused by free radicals, including aging, cancer, diabetes and neurodegenerative diseases. The body has both endogenous and dietary antioxidant systems to protect against free radical damage through catalytic removal of radicals and protection of macromolecules.
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Vitamins are essential organic substances needed by the body in small amounts to perform specific metabolic functions. There are 13 legitimate vitamins that exist as either fat-soluble (A, D, E, K) or water-soluble (C, B-complex). Fat-soluble vitamins are stored in tissues while water-soluble vitamins are not stored and require consistent dietary intake. Deficiencies of vitamins can result in diseases like rickets, osteomalacia, beriberi, and pellagra depending on the specific vitamin lacking in the diet.
Riboflavin,flavoproteins and their clinical applicationsrohini sane
A presentation in lucid-style on Riboflavin (vitamin B2), Flavoproteins and their clinical applications for MBBS , BDS , B Pham and Biotechnology students to facilitate easy leaning.
Vitamin D is an essential vitamin that must be metabolized to become biologically active. It plays an important role in calcium homeostasis, bone and muscle health, immune function, and the regulation of cell growth. The best indicator of vitamin D status is the measurement of 25-hydroxyvitamin D in the blood, as it reflects vitamin D from dietary intake and sunlight exposure. Low vitamin D levels have been associated with increased risk of various chronic diseases. Vitamin D deficiency can lead to impaired bone mineralization and increased fracture risk.
Vitamin D has widespread effects beyond bone health. It acts as a pleiotropic hormone that regulates over 200 genes and has important immunomodulatory properties. Maintaining optimal vitamin D levels may help reduce the risk of infections like tuberculosis and exacerbations of COPD, as well as cancers, cardiovascular disease, fractures and autoimmune disorders. More research is still needed but achieving a serum 25(OH)D level of at least 30 ng/mL through supplementation appears to provide the most benefits.
Vitamin D deficiency is common worldwide and can cause many health issues. It is involved in calcium absorption and bone health. Deficiency leads to osteomalacia and rickets in children, and increases risk of fractures in adults. It may also play roles in cardiovascular disease, diabetes, cancer prevention, autoimmune disease, pregnancy complications, muscle weakness, and mortality. Treatment involves dietary sources of vitamin D, supplementation, and sunlight exposure.
Gran parte delle patologie e dell’invecchiamento degli esseri viventi sono causati da processi chimici ossidativi generati da produzione eccessiva di radicali liberi. La presentazione mostra nello specifico l'impatto dello stress ossidativo sulla riproduzione.
I Radicali Liberi sono prodotti di scarto che si formano naturalmente all’interno delle cellule del nostro corpo quando l’ossigeno è utilizzato nei processi metabolici per produrre energia (ossidazione). Se sono in quantità minima, aiutano il Sistema Immunitario nell’eliminazione dei germi mediante perossidazione lipidica (denaturazione membrane batteriche); mediante un’azione mutagena sul DNA; mediante ossidazione dei Citocromi (arresto respirazione mitocondriale). Se non sono prontamente neutralizzati dai sistemi Antiossidanti, danneggiano i tessuti e le cellule circostanti interrompendo i processi cellulari vitali.
Esiti esame Bioch Siste Umana del 23.01.2017.
Chi volesse rifiutare il voto: scrivere una mail a francesca.re1@unimib.it entro venedì sera. poi i voti saranno registrati senza possibilità di cambiamenti.
Esito esame Biochimica Sist Umana del 13 dicembre 2016.
SOLO chi RIFIUTA il voto: scrivetemi una mail entro domani alle 12. POI i voti saranno registrati.
Proposte stage 2016-2017. In verde: studenti e relativi periodi GIA' ASSEGNATI.
In giallo: studenti e periodi disponibili ANCORA DA CONFERMARE.
I gialli dovrebbero farmi sapere (VIA MAIL) la loro decisione al più presto per eventuale liberazione di posti. grazie.
1. RADICALI LIBERI (RL)
O
SPECIE REATTIVE DELL’OSSIGENO (ROS)
In medicina vengono chiamati radicali
liberi anche i ROS
2. ROS
Definizione
Le specie reattive dell’ossigeno
comprendono:
-Forme parzialmente ridotte
dell’ossigeno (RL)
-Specie chimiche ad alta reattività
3. RADICALE LIBERO
Definizione
Specie chimica capace di esistenza
autonoma contenente uno o più elettroni
spaiati nell’orbitale più esterno
R
ELEVATA instabilità →→ REATTIVITA’
4. ELEVATA instabilità →→ REATTIVITA’
Sottrarre l’elettrone da altre molecole
R + X-H R-H + X propagazione
R + X R-X termine
Formazione di ROS = processo fisiologico
15. OSSIDO NITRICO NO
eNOS
EFFETTI
. anti-aggreganti
. anti-infiammatori
. anti-ipertensivi
. controllo dell’apprendimento
e della memoria
. modulazione delle secrezioni
e della motilità
. modulazione del tono della
muscolatura liscia bronchiale
16. eccessiva produzione di anione
superossido – comportano la
conversione dell’NO in perossinitrito,
una forma radicalica alla quale è legata
la tossicità del mediatore primario
19. FONTI ENDOGENE
Consumo di ossigeno nei mitocondri
Ossidazioni di molecole (es. adrenalina, noradrenalina)
Produzioni da reazioni enzimatiche (es. xantine ossidasi)
RADICALE SUPEROSSIDO O2-∙
Perossisomi
Reazioni SOD-dipendenti
Produzione da reazioni enzimatiche (es. MAO)
Ossidazione acidi grassi
PEROSSIDO DI IDROGENO H2O2
Reazioni ossidoriduttive dell’H2O2
In presenza di ferro libero
RADICALE OSSIDRILE ∙OH
Aumento della temperatura corporea
Aumento delle catecolammine
Produzione di acido lattico
Ipossia-riossigenazione
Fagociti→→→ BURST OSSIDATIVO
26. Velocemente inattivato dalla SOD
No reazioni di propagazione
Velocemente inattivato dalle CAT e GSH
Possibili reazioni di propagazione
27. Tra i ROS è la molecola più tossica
Innesca perossidazione radicalica in tutte le cellule
Danneggia tutte le molecole
Reazioni di propagazione
No meccanismi di inattivazione endogena
DANNI INDOTTI DAI ROS
34. SISTEMI SCAVENGER – spazzini di radicali
Presenti nell’organismo:
ENDOGENI
- Catalasi
-Superossidodismutasi (SOD):
-Glutatione perossidasi
Riciclo del glutatione ossidato:
G-S-S-G + NADPH + H+ 2 GSH + NADP+
(NADPH dalla via dei pentoso fosfati)
Coenzima Q10
Ac. Urico
Bilirubina (prodotti di scarto)
35. La glutatione perossidasi è un enzima
appartenente alla classe delle ossidoreduttasi,
che catalizza la seguente reazione:
L'enzima è una proteina contenente un residuo
di selenocisteina.
38. Il glutatione è un forte antiossidante, sicuramente uno dei
più importanti tra quelli che l'organismo è in grado di
produrre.
Rilevante è la sua azione sia contro i radicali liberi o
molecole come perossido di idrogeno, nitriti, nitrati,
benzoati e altre.
Svolge un'importante azione nel globulo rosso, proteggendo
tali cellule da pericoli ossidativi che causerebbero l'emolisi.
Elemento importante per il suo funzionamento è il NADPH.
39. Il glutatione è un forte antiossidante, sicuramente uno dei
più importanti tra quelli che l'organismo è in grado di
produrre.
Rilevante è la sua azione sia contro i radicali liberi o
molecole come perossido di idrogeno, nitriti, nitrati,
benzoati e altre.
45. VITAMINA E– tocoferolo
RDA 8 mg/die. Più precisamente il fabbisogno andrebbe riferito al contenuto di grassi
poliinsaturi della dieta.
Scarsamente tossica. Tollerata almeno fino a 2000 mg/die.
Svolge azione antiossidante
Contenuto in 100 g di parte edibile (mg)
-------------------------------------------------------------------------------------------------------------------
Vitamina E fegato di bue 0,5
sardine sott’olio 4.3
burro 0,2
olio di semi 4,7
-----------------------------------------------------------------------------------------
carote 0,4
-----------------------------------------------------------------------------------------
albicocche 0,9
mandorle 11,5
3 noci/die
2 mandorle/die
47. VITAMINA C– ascorbato
Parecchi studi mostrano che vit.C diminuisce durante esercizio fisico
Ricerche mostrano che 600 mg vit. C a maratoneti diminuiscono l’incidenza di
infezioni dei tratti respiratori superiori. Alcuni studi mostrano anche un effetto
ergogenico.
Necessità Normali: 60 mg/die.
Allenamento quotidiano: 100 mg
Sport che richiedono sforzi prolungati: fino a 500mg
Quantità superiori vengono eliminate con le urine
Fonti principali Contenuto in 100 g di
parte edibile (mg)
-----------------------------------------------------------------------------------------------------
Vitamina C peperoni 151
broccoletti di rape 110
spinaci 54
pomodori maturi 25
fragole 54
------------------------------------------------
1kiwi 85
1arancia 50
1mandarino 42
1 pompelmo 56
48. La vitamina C previene il raffreddore
E’ una diceria. Non esistono studi che dimostrano una
simile capacità
Esiste una soglia renale ( similmente al glucosio)
Il suo metabolismo produce ossalato (calcoli)
50. VITAMINA A– retinolo
Presente come tale o come precursori non vitaminici (caroteni). Il
contenuto totale viene espresso come retinolo-equivalenti (RE). RDA 1000 RE
Vit. A ha azione antiossidante- Deve essere sconsigliato il sovradosaggio perché si
accumula. Un eccesso porta a diminuzione della densità ossea e aumento del rischio di
fratture dell’anca. Effetti teratogeni sul feto.
I precursori (caroteni) sono deboli antiossidanti in vivo e possono essere pro-ossidanti
nei polmoni. Gli sportivi nelle grandi città dovrebbero introdurre meno carotene con gli
alimenti.
Contenuto in 100 g di parte edibile (mg R.E.)
-------------------------------------------------------------------------------------------------------------------
Vitamina A fegato bovino 16.500
sardine sott’olio 20
burro 960
olio di semi 0
-----------------------------------------------------------------------------------------
carote 1148
zucca 599
spinaci 485
indivia 213
pomodori maturi 135
-----------------------------------------------------------------------------------------
albicocche 360
cachi 237
melone 189
51. Le vitamine funzionano da catalizzatori, cioè aumentano la velocità
delle reazioni biochimiche senza essere consumate. Questo ultimo
fatto spiega perché sono necessarie solo in piccola quantità. Infatti
non si dispone di dati che comprovano la necessità effettiva di un
supplemento vitaminico nello sportivo. Infatti si ritiene che le
maggiori necessità di vitamine possano essere già compensate
dalle maggiori quantità di alimenti introdotti dallo sportivo.
In caso di impegni particolarmente gravosi si può integrare con
vitamine C, E, A, B12-folico.
54. La maggior parte delle patologie e
dell’invecchiamento degli esseri viventi
sono causati da processi chimici
ossidativi, dovuti ad una ECCESSIVA
produzione di radicali liberi.
56. Contribuiscono all’invecchiamento e malattie degenerative
della vecchiaia: tumori, malattie cardiocircolatorie, cataratta,
disfunzioni cerebrali, diminuzione delle difese immunitarie
57. Le proteine presenti negli occhi mostrano un aumento di
solfossido di metionina col passare degli anni e le proteine
nelle cataratte umane presentano più del 60% dei loro residui
di metionina ossidati. Le cavie gravide private di glutatione,
il più importante antiossidante solfidrilico delle cellule,
producono una prole affetta da cataratta.
La più promettente strategia di prevenzione contro questa
patologia consiste nell'aumentare il consumo di antiossidanti
nelle dieta e nel ridurre il fumo.
58. Brain = 2% del peso corporeo
Brain = consuma 20-25% di tutto l’ossigeno inspirato
59.
60. Danno microvascolare => attivazione fosfolipasi C
Accumulo e attivazione di neutrofili
Emolisi
Riduzione ossigeno (ipossia)
62. Nel caso di intossicazione acuta di etanolo, è probabile che
l’eccesso di acetaldeide che si forma venga ossidata da alcuni
enzimi alternativi (xantina-ossidasi) con produzione di anione
superossido.
