biochem vitamins

1. VITAMINS AND
MINERALS
GROUP MEMBERS:
 SHALVIN NAND
 NIKIL CHAND
 SHAMAL KUMAR
 SHIVNESH SOBHA
 ANGIE

2. OBJECTIVES
• DEFINE VITAMIN, COFACTOR AND MINERALS
• DESCRIBE THE FUNCTION OF VITAMINS AND COFACTORS
AND MINERALS,
• PROVIDE EXAMPLES OF EACH GROUP. (CLASSIFICATION)
• DISEASES ASSOCIATED WITH VITAMINS AND MINERALS
• UTILIZATION OF MINERALS AND VITAMINS

3. INTRODUCTION
• Vitamins and minerals are MICRONUTRIENTS.
• Micronutrients are needed only in minuscule amounts, these
substances are the “magic wands” that enable the body to produce
enzymes, hormones and other substances essential for proper
growth and development.
• However, the consequences of their absence are severe.
• Iodine, vitamin A and Iron are most important in global public
health terms; lacking those represents a major threat to the
health and development of populations, particularly children and
pregnant women in low-income countries. (WHO, 2018)

4. • A variety of micronutrients are required in a healthy diet,
as they act as cofactors integral to the enzymes involved
in cell functions like DNA and protein synthesis, cell
proliferation, immunity, and anti-oxidation processes

5. • Vitamins and minerals are micronutrients.
• Are group of organic molecule and is an essential micronutrient
that cannot be synthesized in the body.
• are needed in small quantities for the proper functioning of its
metabolism.
• are obtained from diet and stored in liver
• Perform specific cellular functions
• Disease prevention

9. VITAMIN A

10. VITAMINA
• Vitamin A is a group of unsaturated nutritional organic
compounds
• Vitamin A refers to three biologically active vitamers
Retinol
Retinal
Ritinoic acid
• Also some refers to several provitamin carotenoids
(most notably beta-carotene)

11. CONTINUED….
• They are polysioprenoid compounds compromising two
distinct component
A cyclohexnyl ring
A side chain
• A side chain is made up of several isoprene units, which
is attached the cyclohexenyl ring

12. STRUCTURE

13. FUNCTION
Development of healthy skin and nerve tissue.
Aids in building up resistance to infection.
Functions in eyesight(retinal) and bone formation.(retinoic Acid)
It is important in the ration of pregnant females.(retinol)

14. ABSORPTION
B-CAROTENE
• Absorbed in small intestine and enters mucosal cells where it
is cleaved into two molecules of trans-retinal dioxygenase
and molecular oxygen
• Bile salts facilitates the reaction
• Retinal is oxydised to retinol by an NADH or NADPH-
dependent retinal reductase
• Retinol is esterified with a fatty acid, incorporated into
chylomicrons together with dietary lipids, and secreted into
lacteals

15. RETINOL ESTERS
• Hydrolyzed in the intestinal lumen by pancreatic enzyme
called carboxylic ester hydrolase
• The free retinol generated is transferred across mucosal
cell
• Then esterified , incorporated into chylomicrons and
secreted into lacteals.
• Note: the presence of lipids in the intestine ensures
efficient absorption of retinol

16. TRANSPORT ANDSTORAGE
• Vitamin A is released from the liver as retinol
• Zn is essential for retinol metabolism
• Retinol is transported in the circulation by the retinol
binding protein(RBP) in association with pre-albumin
• One molecule of RBP binds one molecule of retinol
• The retinol-rbp complex binds to specific receptors on
the cell membrane of peripheral tissue and enters the
cells

17. • Many cells of target tissues contain a cellular retinol-binding
protein (CRBP) that carries retinol to the nucleus and binds to
the chromatin (DNA)
• Retinol exerts its function in a manner to that of a steroid
hormone
• Retinoic acid is mainly transported in the blood by binding to
albumin
• Small amounts of retinoic acid in the blood is also transported in
combination with aporetinol binding protein

18. VITAMINA ANDVISION
• Rodopsin synthesis
• WALDS visual cycle
• Regeneration of 11-cis-retinal
• Dark adaptation mechanism
• Mechanism of vision

20. OTHER FACTORS OF VITAMIN A
• Regulation of gene expression
• Growth and differentiation
• Glycoprotein synthesis
• Reproduction
• Antioxidant

21. SOURCES
Whole milk, carotene, animal body oils (cod fish
and tuna), legume forages and can be synthetically
produced.

23. TOXICITY
• More than 300mg causes hypervitaminosis
• Symptoms: dry and pruritic skin, hepatomegaly, increase
intracranial pressure
• It can cause malformation of growing fetus

24. DEFICIENCY SIGNS
Retarded growth in the young
The development of a peculiar condition around the eyes
known as xerophthalmia
Night blindness
Reproductive disorders.

25. DISEASES
• EYE DISEASES
• POOR IMMUNITY
• ANEMIA
• POOR HAIR HEALTH
• POOR SKIN HEALTH

26. VITAMIN D

27. VITAMIN D
• Vitamin D refers to a group of fat-soluble secosteroids.
• Most important compounds in this group are
vitamin d3 - cholecalciferol
vitamin d2 – ergocalciferol
• Synthesis of vitamin D in the skin is the major natural source
of the vitamin
• Vitamin D from the diet or dermal synthesis from sunlight is
biologically inactive; activation requires enzymatic
conversion (hydroxylation) in the liver and kidney

28. STRUCTURE

29. FUNCTION
• is essential for the proper utilization of calcium and
phosphorus to produce normal, healthy bones.

30. ABSORPTION
• Diet from animal sources such as animal liver contains vitamin D3
• Diet from plant sources contains vitamin D2
• Absorption: vitamin D2 and D3 are absorbed from upper small
intestine and bile is essential
• Mechanism: vitamin D3 and D2 form mixed micelles by combining
with bile salts (micelles)
• Mixed micelles are presented to mucosal cells
• Absorption occurs by passive transport

31. TRANSPORT
• Vitamin D binding globulin: vitamin D is transported from
intestine to the liver by binding to vitamin D binding
globulin
• 25 – hydroxy D3 and 1,25 – dihydroxy D3 are also
transported in the blood by binding to vitamin D binding
globulin
• Storage: 25 – hydroxycholecalciferol is the major storage
and circulatory form of vitamin D

32. VITAMIN D AND SUNSHINE
• During the course of cholesterol biosynthesis 7-
dehydrocholesterol is formed as an intermediate
• On exposure to sunlight, 7-dehydrocholesterol is converted
to cholecalciferol in the skin (dermis and epidermis)
• Dark skin pigment (melanin) adversely influences the
synthesis of cholecalciferol

33. • Skin is the largest organ in the body
• The production of vitamin D in the skin is directly
proportional to the exposure to sunlight and inversely
proportional to the pigmentation of skin
• Excessive exposure to sunlight does not result in vitamin D
toxicity since excess provitamin D3 are destroyed by
sunlight itself

34. CALCITRIOL METABOLISM
• Active form: the active form of vitamin D is 1,25 –
dihydroxycholecalciferol and is also called as calcitriol
• Cholecalciferol is first hydroxylated at 25thp osition to 25 –
hydroxycholecalciferol by a specific hydroxylase present in
liver
• Kidney possesses a specific enzyme, 25 –
hydroxycholecalciferol 1 – hydroxylase

35. CONTINUED
• 25 – hydroxycholecalciferol 1 – hydroxylase hydroxylates
25 – hydroxycholecalciferol at position 1 to produce 1,25
dihydroxycholecalciferol (1,25-DHCC)
• 1,25 – DHCC contains 3 hydroxyl groups (1, 3,25) and
called as calcitriol
• Both hydroxylase enzymes (of liver and kidney) require
cytochrome P450, NADPH and molecular oxygen for
hydroxylation process

36. REGULATION
• Formation of 1,25 – DHCC is regulated by the regulation of
renal 1 α – hydroxylase
• 1 α – hydroxylase activity is increased by hypocalcemia
• Hypocalcemia stimulates PTH secretion which, in turn,
increases 1 α – hydroxylase
• 1 α – hydroxylase activity may be feedback inhibited by
1,25 – DHCC

38. SOURCES
•Whole milk
•Sun-cured hays
•Forage crops
•Fish liver oils
•Irradiated yeast.

40. DEFICIENCY SIGNS
•Retarded growth
•Misshapen bones (rickets),
•Lameness and osteoporosis.

41. •DISEASE
• Rickets can be caused by lack of sunlight, but
also from insufficient calcium. Vitamin D
linked to calcium absorption.(Rickets
reported in NYC.)

43. WHAT IS VITAMIN E?
• VITAMIN E IS FOUND NATURALLY IN SOME FOODS, ADDED TO OTHERS, AND
AVAILABLE AS A DIETARY SUPPLEMENT.
• “VITAMIN E” IS THE COLLECTIVE NAME FOR A GROUP OF FAT-SOLUBLE
COMPOUNDS WITH DISTINCTIVE ANTIOXIDANT ACTIVITIES.
• ALPHA- (OR Α-) TOCOPHEROL IS THE ONLY FORM THAT IS RECOGNIZED TO
MEET HUMAN REQUIREMENTS.
• ALSO KNOWN AS A BEAUTY VITAMIN

44. STRUCTURE
COLLECTIVE VITAMIN E
COMPOUNDS

45. SOURCES OF VITAMIN E
 Numerous foods provide vitamin E
 Nuts, seeds, and vegetable oils are among the best sources of
alpha-tocopherol
 Significant amounts are available in green leafy vegetables and
fortified cereals

48. BENEFITS
THICKENS HAIR

49. MUSCLE
STRENGTH

50. RDA – VITAMIN E
• AVERAGE DAILY LEVEL OF INTAKE SUFFICIENT TO MEET THE NUTRIENT
REQUIREMENTS OF NEARLY ALL (97%–98%) HEALTHY INDIVIDUALS; OFTEN USED
TO PLAN NUTRITIONALLY ADEQUATE DIETS FOR INDIVIDUALS.

51. BIOCHEMICAL FUNCTIONS
 Most of the functions of Vit. E are related to its antioxidant
properties
1. Essential for membrane structure and integrity of the cells
2. Increases the synthesis of heme by enhancing ALA synthase and ALA
dehydratase
3. Required in cellular respiration- stabilizes co-enzyme Q in ETC
4. Works in association with Vitamin A, C and beta carotene- to prevent
cataracts.
5. Prevents oxidation of LDL.

52. ABSORPTION- MICELLE DEPENDENT PASSIVE
DIFFUSION

53. METABOLISM

54. TOXICITY- HYPERVITAMINOSIS
• VITAMIN E IS KNOWN AS A NONTOXIC SUBSTANCE IN NATURE
• HOWEVER, AT VERY HIGH DOSES, IT CAN ANTAGONIZE THE FUNCTIONS OF OTHER
FAT SOLUBLE VITAMINS
• MORE THAN 1000 IU PER DAY, LEADS TO:
• HEADACHE
• NAUSEA
• DOUBLE VISION
• MUSCLE WEAKNESSES
• GASTROINTESTINAL DISTRESS
 CONTRAINDICATION: DUE TO COAGULANT DEFECT ( VITAMIN K DEFICIENCY)

55. VITAMIN E DEFICIENCY
• ATAXIA
• SKELETAL MYOPATHY
• RETINOPATHY
• HAIR LOSS

57. WHAT IS VITAMIN K?
• IS THE ONLY FAT SOLUBLE VITAMIN WITH A SPECIFIC COENZYME FUNCTIONS
• PHYLLOQUINONE IS THE MAIN DIETARY FORM OF VITAMIN K

58. STRUCTURE

59. SOURCES OF VITAMIN K

62. RDA- VITAMIN K

63. TOXICITY

64. ABSORPTION
• SIMILAR TO VITAMIN E
• ABSORPTION TAKES PLACE IN THE SMALL INTESTINE IN THE PRESENCE OF BILE
SALTS
• THE TRANSPORTATION IS CARRIED OUT THROUGH CHYLOMICRONS
• STORAGE OCCURS IN LIVER AND FROM LIVER IT IS TRANSPORTED TO
PERIPHERAL TISSUES IN BOUND WITH VLDL

65. BIOCHEMICAL FUNCTIONS

67. ANTAGONIST

68. VITAMIN K AS A COFACTOR
• VITAMIN K IS THE COFACTOR FOR THE CARBOXYLATION OF GLUTAMATE
RESIDUES IN THE POST SYNTHETIC MODIFICATION OF PROTEINS TO FORM
GAMMA-CARBOXYGLUTAMATE

69. SYNTHESIS OF BONE CALCIUM- BINDING
PROTEINS

70. VITAMIN K DEFICIENCY

71. OSTEOPOROSIS
• OSTEOPOROSIS, A DISORDER CHARACTERIZED BY POROUS AND FRAGILE BONES
• SIMPLY WEAK BONES

75. NIACIN – VITAMIN B3
• ALSO CALLED NICOTINIC ACID
• ODORLESS WHITE CRYSTALLINE SUBSTANCE
• STRUCTURAL COMPONENT OF NAD AND NADP DEHYDROGENASE COFACTOR
• RESISTANT TO HEAT AND OXIDATION
• STABLE VITAMIN
STRUCTURE
 PYRIDINE DERIVATIVE
 SIMPLE STRUCTURE WITH MOLECULAR FORMULA- C6H5O2N

77. FUNCTIONS
• RELEASE OF ENERGY
• SYNTHESIS OF FATS AND PROTEIN
• ACT AS COENZYME
• REDOX REACTION
• VASODILATION
• NON REDOX REACTIONS

78. DEFICIENCY AND CLINICAL CORRELATION
• DUE TO INSUFFICIENT INTAKE OF FOOD
• ALCOHOLISM
• TRYPTOPHAN ABSORPTION DISORDER
• MALABSORPTION SYNDROME
NORMAL RANGE – 0.50-0.85UG/ML
RDA
MEN – 16MG/DAY
WOMEN – 14MMG/DAY
DEFICIENCY OF NIACIN LEADS TO PELLAGRA

79. PELLAGRA
• ARISES DUE TO NIACIN DEFICIENCY
• CHARACTERIZED BY 4 D’S
DERMATITIS
DIARRHEA
DEMENTIA
DEATH

80. TOXICITY
• MEDICALLY USED TO LOWER LDL AND TRIGLYCERIDE
• INCREASES HDL
TOXICITY OCCURS WHEN NIACIN INTAKE IS MORE THAN 1000MG/DAY
SYMPTOMS OF TOXICITY
 TACHYCARDIA
 ITCHING
 GOUT
 ABDOMINAL PAIN

82. PANTOTHENIC ACID- VITAMIN B5
• PANTOTHEN- MEANS EVERYWHERE
• WATER SOLUBLE
• CHICK ANTI-DERMATITIS FACTOR
STRUCTURE
 PANTOIC ACID JOINED TO BETA ALANINE
 HELD BY PEPTIDE BOND
 HEAT STABLE
 ACTIVE FORM – CO ENZYME A (COA)

83. ABSORPTION AND TRANSPORT
• FOOD –CONTAINS ACETYL COA AND PHOSPHOPANTOTHEINE
• INTESTINAL PYRO PHOSPHATASE HYDROLYZE TO YIELD FREE FORMS
• FREE FORMS ARE ABSORBED
TRANSPORT
ENTERS THE PORTAL CIRCULATION
MOSTLY ENDS UP IN LIVER

84. SYNTHESIS OF COA ( ACTIVE FORM)
• PANTOTHENIC ACID IS PHOSPHORYLATED- 4 PHOSPHOPANTOTHENIC ACID IS
FORMED
• 4-PHOSPHOPANTOTHENIC ACID IS CONVERTED TO
4-PHOSPHOPANTOTHENYLCYSTEINE
• 4-PHOSPHOPANTOTHENYLCYSTEINE IS DECARBOXYLATED TO 4-
PHOSPHOPANTOTHEINE
• 4-PHOSPHOPANTOTHEINE IS THEN CONVERTED TO DIPHOSPHO COENZYME
• PHOSPHORYLATION OF DIPHOSPHO CO ENZYME YIELDS THE ACTIVE CO ENZYME
A (COA)

85. COENZYME A STRUCTURE

87. FUNCTIONS
Function is mostly related to CoA
 Involved in most of the metabolism
 Acts as co-factor as in:
Pyruvate dehydrogenase complex
α-ketoglutarate dehydrogenase
FAS complex
Thiolase, HMG COA synthase
 Helps in formation of neurotransmitters
 Act as substrates
 Essential for energy metabolism

88. DEFICIENCY AND CLINICAL CORRELATIONS
• DEFICIENCY IS VERY RARE
• USUALLY IN MALNOURISHED INDIVIDUALS
• ANOREXIA NERVOSA
• MALABSORPTION SYNDROME
NORMAL RANGE:1.6 TO 2.7 MCMOL/L
 NO TOXICITY ARISES DUE TO EXCESSIVE INTAKE OF PANTOTHENIC ACID
RDA
ADULTS : 10MG/DAY
CHILDREN : 7MG/DAY

89. CLINICAL SYMPTOMS
• Hypoglycemia
• Irritation
• Fatigue
• Tiredness
• Depigmentation of hair

91. BIOTIN (VITAMIN B7)
• PRESENT IN MITOCHONDRIA AND CYTOSOL
• ESSENTIAL FOR CELL GROWTH
• SYNTHESIZED BY FUNGI, BACTERIA AND YEAST
STRUCTURE
 MEMBER OF B COMPLEX GROUP OF VITAMIN
 APPEARS AS WHITE CRYSTALLINE NEEDLE
 SULPHUR CONTAINING
 2 CONDENSED HETEROCYCLE (IMIDAZOLIDINE ANDTHIOLANE)
 SIDE CHAIN OF VALERIC ACID

92. FUNCTIONS
• Carboxylation reaction
Required for enzyme
Pyruvate carboxylase
Acetyl CoA carboxylase
Propionyl carboxylase
*NOT ALL CARBOXYLATION
REACTION REQUIRES BIOTIN

93. ABSORPTION OF BIOTIN
• INTESTINAL PROTEASE YIELDS BIOTINYLLYSINE
• INTESTINAL BIOTIN AMIDE AMINO HYDROLASE LIBERATES FREE BIOTIN
• FREE BIOTIN IS ABSORBED IN PROXIMAL PART OF SMALL INTESTINE
2 ABSORPTION MECHANISM INVOLVED:
FACILITATED TRANSPORT
PASSIVE DIFFUSION

95. DEFICIENCY AND CLINICAL FEATURES
• DEFICIENCY IS VERY RARE
CLINICAL FEATURES
 SEVERE DERMATITIS
 WEAKNESS
 NAUSEA
 ALOPECIA
 LOSS OF APPETITE
 MUSCLE PAIN
 WEAKNESS
NORMAL BLOOD BIOTIN LEVEL 400-1200NG/L
<400NGL – DEFICIENT STATE

96. CAUSE OF DEFICIENCY
• POOR PARENTERAL NUTRITION
• CONSUMING RAW EGG
• BIOTINIDASE DEFICIENCY

97. TOXICITY
• TOXICITY IS RARE
• CAN OCCUR DURING PROLONG OVERDOSE OF BIOTIN
CLINICAL SYMPTOMS INCLUDES
SKIN RASHES
SLOWER RELEASE OF INSULIN
LOWER VITAMIN C AND VITAMIN B6 LEVEL
HIGH BLOOD SUGAR LEVEL

99. ASCORBIC ACID - VITAMIN C
water soluble vitamin
Acidic in nature
Is a strong reducing agent
Cannot be synthesized by humans
Present in all tissues as reduced form
Oxidation occurs in presence of copper
Mostly present in retina, thymus and adrenal gland

100. STRUCTURE
• HEXOSE DERIVATIVE
• MONOSACCHARIDE IN STRUCTURE
• 2 FORMS
L- ASCORBIC ACID
L-DEHYDRO ASCORBIC ACID
 D-ASCORBIC ACID IS BIOLOGICALLY INACTIVE

101. IRON AND HEM METABOLISM
ACT AS COFACTOR
BONE FORMATION
FORMATION OF NOREPINEPHRINE

102. FUNCTIONS
MATURATION OF ERYTHROCYTES
STEROID SYNTHESIS
IMMUNOLOGICAL FUNCTION
REDUCES CATARACT FORMATION
ANTIOXIDANT FUNCTION

103. FOOD SOURCE
 LEMON
 ORANGE
 GRAPES
 TOMATOES
 SPINACH
RDA
ADULTS - 60MG/DAY
PREGNANCY - 80MG/DAY

104. DEFICIENCY AND CLINICAL CORRELATION
OCCURS DUE TO:
DIETARY DEFICIENCY-ANOREXIA NERVOSA
IMPAIRED ABSORPTION
DEFICIENCY LEADS TO SCURVY
NORMAL SERUM LEVEL- 0.3-0.6MG/DL

105. SCURVY
• Occurs in case of vitamin C deficiency
Clinical signs
 bleeding gums and hemorrhage
 small skin discoloration due to ruptured blood vessels
 easy bruising,
 impaired wound and fracture healing
 joint pain
 loose and decaying teeth
 hyperkeratosis of hair follicles
 koilonychias
BARLOWS DISEASE-refers to scurvy in infants(below 12 months

106. TOXICITY
• RARE AS EXCESS IS EXCRETED IN URINE
• MORE THAN 2000MG MAY CAUSE IRON OVERLOAD-HEMOCHROMATOSIS
• EXCESS VITAMIN C CAN CAUSE:
NAUSEA
VOMITING
DIARRHEA
HYPEROXALURIA AND KIDNEY STONES

107. REFERENCES
• Dermaharmony.Com. (2017). Macronutrients and micronutrients. [Online] available at:
https://www.Dermaharmony.Com/skinnutrition/macronutrientsmicronutrients.Aspx
[accessed 29 AUG. 2018].
• Ods.Od.Nih.Gov. (2018). Office of dietary supplements - vitamin E. [Online]
available at: https://ods.Od.Nih.Gov/factsheets/vitamine-
healthprofessional/#h4 [accessed 14 sep. 2018].
• Murray. R. K, et al, 2012. Harper’s illustrated biochemistry. Ed 29. Mcgraw hill
companies. Usa
• Ods.Od.Nih.Gov. (2018). Office of dietary supplements - vitamin K. [Online]
available at: https://ods.Od.Nih.Gov/factsheets/vitamink-
healthprofessional/#h3 [accessed 30 sep. 2018].