VITAMINS INFO GRAPHICS

Catalogued by Ali Raza Chaudary

N67 | NISHTAR MEDICAL UNIVERSITY MULTAN

BIBLIOGRAPHY:

1. Lippincott Illustrated Reviews Biochemistry 7th Ed. Chapter 28

2. Harper’s Illustrated Biochemistry 30th Ed. Chapter 44
3. Internet Sources
a. http://www.fda.gov/nutritioneducation
b. https://lpi.oregonstate.edu/mic/vitamins
 CONTENTS 2
DESCRIPTION PAGE NO
Vitamins 3
Difference between Water Soluble and Fat Soluble Vitamins 3
Classification of Vitamins 4
Vitamin A 5
Vitamin D 7
Vitamin E 9
Vitamin K 10
Vitamin C 11
Vitamin B1 12
Vitamin B2 13
Vitamin B3 14
Vitamin B5 15
Vitamin B6 16
Vitamin B7 17
Vitamin B9 18
Vitamin B12 20
 VITAMINS 3
Vitamins are chemically unrelated organic compounds that cannot be synthesized in adequate quantities by humans and, therefore, must be
supplied by the diet.
EXCEPTIONS:
SYNTHESIZED BY THE BODY SYNTHESIZED IN THE BODY
(BY BACTERIAL CELLS) (BY BODY CELLS)
VITAMIN NAME SYNTHESIZED BY VITAMIN NAME SYNTHESIZED IN
Menoquinones (Vitamin K2) Intestinal bacteria Cholecalciferol (Vitamin D) In skin by sunlight
Cobalamine (Vitamin B12) Microorganisms Niacin (Vitamin B3) In body from essential amino
acid tryptophan
Biotin (Vitamin B7) In body by intestinal flora
Carotenes (Vitamin A) In body cleaved to retinoids

DIFFERENCES BETWEEN WATER & FAT

SOLUBLE VITAMINS
FEATURE WATER-SOLUBLE VITAMINS FAT-SOLUBLE VITAMINS
Solubility Water Fat or organic solvents
Absorption Directly into the blood from intestine First into the lymph, then the blood.
Digestion Easily Requires bile and fat
Transport Travel freely Many require protein carriers
Storage Not stored except Vitamin B2 & B12 but circulate Stored in body fat depots and livers by
freely in water-filled parts of the body. chylomicrons
Excretion Via urine and more readily Via faeces and less readily
Toxicity Usually non toxic as they are readily excreted in Likely to reach toxic levels when consumed from
urine except Vitamin B6. supplements.
Requirements Needed in frequent doses. (1-3 days) Needed in periodic doses. (weeks/months)
Coenzymes Act as coenzymes Do not act as Coenzymes except Vitamin K
Deficiency Faster onset Slower onset
CLASSIFICATION OF VITAMINS 4
 VITAMIN A 5
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Retinol (preformed vitamin A) Retinol 900 μg 700 μg 770 μg 900 μg Retinol and Retinyl esters:
Retinal (aldehyde derivative) Retinal Liver & Kidney
Retinoic Acid (acid derivative) Retinoic Acid Butter & Egg Yolk
β-Carotene (provitamin A) Carotenes:
Yellow, orange, dark green vegetables & fruits.
ABSORPTION TRANSPORT SECRETION STORAGE
In enterocytes as retinol derived from: Reesterification of retinol to Retinyl Retinol by liver in association with Retinyl esters (retinyl palmitate) in liver
Hydrolysis of retinyl esters esters from intestine in chylomicrons plasma retinol binding proteins and and adipose tissue
Reduction of retinal (from transthyretin
cleavage of β-carotenes)
THERAPEUTIC TOXICITY & HYPER-
DIETARY ACTIONS DEFICIENCY
ACTIONS VITAMINOSES
Cell Differentiation & Gene Expression Tretinoin NYCTALOPIA
All forms involved (All-Trans retinoic acid)
UL = 3000 μg/day
Night Blindness due to increased visual threshold
Retinol oxidized to retinoic acid and Not administrated orally IRREVERSIBLE LOSS OF VISUAL CELLS >7.5 mg/day Retinol
bind RAR, expressing gene, recruiting  Mild acne Due to prolonged deficiency Skin: Reflections, Dry and Pruritic
activators and repressors, regulating  Skin aging
retinoid specific RNA synthesis  Acute promyelocytic
XEROPHATHALMIA due to decreased keratin
Pathological dryness of conjunctiva and cornea synthesis
Visual Cycle leukemia
due to increased keratin synthesis resulting from Liver: Enlarged and cirrhotic
All forms except retinoic acid Isotretinoin
severe deficiency CNS: Rise in intracranial pressure
11-cis retinal + Opsin = Rhodopsin (13-Cis retinoic acid)
BLINDNESS Pregnancy: Teratogenesis
(Both rod & cone cells) Administrated orally
Reproduction  Severe cystic acne Untreated xerophthalamia leading to corneal
ulceration forming opaque scar tissue >Isotretinoin
All forms except retinoic acid support Synthetic Retinoid
IMPAIRED IMMUNE FUNCTIONS Pregnancy: Teratogenesis
spermatogenesis and prevent fetal Administrated orally
Cardiovascular Diseases
resorption  Psoriasis (skin condition Retinol bonding protein is negative acute phase
Increased Cholesterol &
Growth that speeds up the life protein i.e. reduced in infection, decrease conc.
triacylglycerides
Mucus Secretion cycle of skin cells) of circulating vitamin A.
Immune Function
RBC, Skin & Bone Formation
Antioxidant (β-carotenes)
METABOLISM OF VITAMIN A 6
 VITAMIN D 7
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Ergosterol (Provitamin D2) 1,25-Dihydroxy- 10-15 10-15 5 mg 5 mg Endogenous Vitamin Precursor:
7–Dehydrocholesterol cholecalciferol mg mg Conversion of 7-dehydrocholestrol to choleacalciferol in presence of
(Provitamin D3) (calcitriol) UV radiations of sunlight in dermis and epidermis of skin.
Ergocalciferol (Vitamin D2) Ergocalciferol (Vitamin D2):
Cholecalciferol (Vitamin D3) Plants
Cholecalciferol (Vitamin D3):
Animal tissues (Fatty fish & liver & Egg Yolk)
Artificially fortified milk
ABSORPTION &
TRANSPORT SECRETION STORAGE
FORMATION
Vitamin D Formation Transported from intestine in Inactive form of vitamin D undergoes 25--diOH-D3 (Calcidiol) in liver and
In dermis and epidermis of skin chylomicrons to blood into the liver hydroxylation by 25-hydroxylase in liver adipose tissue
Absorption then taken to kidney where again
Absorbed from enterocytes as it hydroxylated by 1-hydroxylase to give
also require bile salts and fats for active form of vitamin D i.e 1,25-diOH-
absorption D3 (calcitriol). Major dominant form in
blood is 25--diOH-D3 (Calcidiol).
TOXICITY & HYPER-
DIETARY ACTIONS DEFICIENCY
VITAMINOSES
Maintain adequate serum levels of Ca. RICKETS (in children)
1. By increasing uptake of Ca by
UL = 100 μg/day
Continued formation of collagen matrix of bone but incomplete mineralization Loss of appetite
intestine results in soft and pliable bones
Calcitriol + Cystosolic Receptor = Nausea
OSTEOMALACIA (in adults) Thirst
1,25-diOH-D3-receptor complex
Demineralization of preexisting bones increases their susceptibility to fractures Weakness
which regulate gene expression of
calbindin i.e. Ca-binding protein RENAL OSTEODYSTROPHY Metastatic Calcification: Enhanced
2. By minimizing loss of Ca by kidney Chronic Liver Disease  Less Active Vitamin D  Increased retention of PO43- Ca absorption and bone
increasing reabsorption Hyperphosphatemia & Hypocalcemia demineralization leading to
3. By stimulating demineralization of Therapy: Supplementation of Vitamin D accompanied by PO43- reduction hypercalacemia resulting in
bone when blood Ca is low HYPOPARATHYROIDISM deposition of Ca salts in soft tissues
Lack of PTH Hyperphosphatemia & Hypocalcemia Toxicity is due to dietary supplements
Therapy: Supplementation of Vitamin D accompanied by Calcium not because of skin formation of vit. D
METABOLISM OF VITAMIN D 8
 VITAMIN E 9
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Tocopherols (8 in number) α-tocopherol 15 mg 15 mg 15 mg 16 mg Rich sources:
Tocotrienols Vegetable Oils
Other sources:
Liver and Eggs
ABSORPTION &
TRANSPORT SECRETION STORAGE
REGENERATION
Vitamin E Regeneration Transported from intestine in α-Tocopherol is secreted in association α-Tocopherol in liver, muscle and
By vitamin C during antioxidant activity chylomicrons to blood into the with very low density lipoprotein (VLDL) adipose tissue (90% in adipose tissue)
Absorption liver from the liver.
In enterocytes as α-tocopherol as it also
require bile salts and fats
TOXICITY & HYPER-
FUNCTIONS DEFICIENCY
VITAMINOSES
Major Lipid-Soluble Antioxidant in Cell Membranes
Due to Abetalipoproteinemia: Caused by defect in formation of
& Plasma Lipoproteins chylomicrons
UL = 1000000
Vitamin E + Lipid peroxide radical New born and Infants μg/day
  Low reservoirs of Vitamin E
 Breast milk contain vitamin
Tocopheroxyl Radical No toxicity
 Supplements are given to prevent hemolysis and retinopathy
 associated with vitamin E deficiency
Reduced back to Tocopherol by vitamin C Adults:
  Resorption of Fetuses
 Testicular Atrophy
Resultant Stable Monodehydroascrobate Radical
 Nerve and Muscle Membrane Damage: People suffereing from
 severe fat malsorption, cystic fibrosis and Chronic Liver Diseases
Enzymatic/Non-enzymatic Actions as they cannot absorb or transport it.
  Hemolytic Anemia: Fragile RBC membranes as result of lipid
peroxidation
Ascorbate and Dehydroascorbate
Not recommended for prevention of chronic disease such as CVD or
Boosts Immune Function
cancer, it may lead to more severe CVD and stroke.
 VITAMIN K 10
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Phylloquinone (Vitamin K1) – Phylloquinone 120 μg 90 μg 90 μg 90 μg Internal Sources: Vitamin K2
plants Menaquinone By gut microorganims
Menaquinone (Vitamin K2) – Menadione External Sources: Vitamin K1
intestinal bacteria Cabbage, Kale, Spinach
Menadione (Synthetic Egg Yolk & Liver
preformed Vitamin K2)
ABSORPTION &
TRANSPORT SECRETION STORAGE
FORMATION
Vitamin K Formation Transported from intestine in Secreted in association with low density Stored in liver, and adipose tissue mostly
Menaquinone by intestinal bacteria chylomicrons to blood into the lipoprotein (LDL) from the liver mostly as as Phylloquinone.
(10% Vitamin K) liver mostly as Phylloquinone. Phylloquinone.
Absorption
In enterocytes as Phylloquinone mostly
it also require bile salts and fats
TOXICITY & HYPER-
DIETARY ACTIONS DEFICIENCY
VITAMINOSES
Synthesis of Blood Clotting Proteins True deficiency is unusual
 Formation of γ-carboxyglutamate (Gla)
UL = Not Set
HYPOPROTHROMBINEMIA
 Carboxylation of several glutamic acid residues to Gla  Intestinal population is reduced by antibiotics as INFANTS
residues for synthesizing Prothrombin (FII), FVII, FIX, FX in debilitated geriatric patients Toxic effects on RBC membranes
 It requires γ-glutamyl carboxylase, O2, CO2 and  By cephalosporin antibiotics (cefamanadole), Hemolytic Anemia
hydroquinone form of Vitamin K (which get oxidized to by warfarin like mechanism that inhibits VKOR Jaundice
epoxide form in presence of VKOR) Bones Affected
 VKOR (vitamin K epoxide reductase) is inhibited by Warfarin Deficiency in Infants ADULTS
 It is also present in osteocalcin, matrix Gla protein of bone  Sterile intestines Rare
and Protein C and S  Human milk contains 1/5 of daily requirements
 Interaction of Prothrombin with membranes of vitamin K
Prothrombin binds negatively charged phospholipids of  Single intramuscular dose of vitamin K as
damaged endothelium and platelets  Increases rate at prophylaxis against hemorrhage disease of new
which proteolytic conversion of prothrombin to thrombin born.
occurs
 VITAMIN C 11
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Ascorbic Acid Ascorbic Acid 90 mg 75 mg 85 mg 120 mg Citrus fruits and juices (e.g., oranges and grapefruit)
Monodehydro Ascorbic Acid Kiwifruit
Dehydro Ascorbic Acid Peppers
Strawberries
ABSORPTION TRANSPORT STORAGE TOXICITY HYPERVITAMINOSES
Absorption decreases with intake Primarily in free form None None Beneficial
Oxidized prior to absorption in small intestine by Sodium Enhance absorption of inorganic Fe
Dependent Co-Transporters (SVCT1 & SVCT 2) Prevent Common Cold

DIETARY ACTIONS DEFICIENCY

Non-enzymatic Effects due to its action as reducing agent and oxygen radical quencher SCURVY
Antioxidant with Vitamin E and β-carotenes preventing many Chronic Diseases as CVD and certain cancer  Sore and spongy gums
Immune function  Loose teeth
Wound healing  Fragile blood vessels
Absorption of dietary non-heme Fe from intestine by reduction of ferric form  Hemorrhage
Collagen formation & Maintenance of connective tissue  Swollen joints
Coenzymes for 2 types of hydroxylases i.e Copper-containing hydroxylases & Iron-containing hydroxylases  Bone changes
TYPE NAME ROLE  Fatigue
Copper Dopamine-β-hydroxylase Synthesis of catecholamine (epinephrine and non-epinephrine) from  All due to defective collagen
containing tyrosine in CNS and adrenal medulla formation
Cu+1  Cu+2 Vit.C Cu+1-OH MICROCYTIC ANEMIA
Peptidylglycine hydroxylase Hydroxylation of alpha carbon of glycine  Due to poor absorption of iron
Cu+1  Cu+2 Vit.C Cu+1-OH from intestine
Iron Proline Hydroxylase Formation of osteocalcin
containing Formation of C1q component of complement
Postsynthetic modification of procollagen to collagen
Lysine Hydroxylase Postsynthetic modification of procollagen to collagen
Aspartate-β-hydroxylase Postsynthetic modification of precursor of protein C, Vitamin K
dependent protease that hydrolyzes activated FV in blood clotting
Trimethyllysine hydroxylase Synthesis of carnitine
γ-Butyrobetaine hydroxylase
 VITAMIN B1 12
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Thiamine Thiamine 1.2 mg 1.1 mg 1.4 mg 1.4 mg Legumes (Beans, Peas, Lentils)
Thiamine monophosphate (TMP) pyro- Whole Grain (Cereal, Oats, Barley, Wheat)
Thiamine diphosphate (TDP)/(TPP) phosphate Nuts
Thiamine triphosphate (TTP), (TPP)/(TDP) Sunflower seeds
Adenosine thiamine triphosphate (ATTP)
Adenosine thiamine diphosphate (ATDP)
ABSORPTION TRANSPORT STORAGE TOXICITY STATUS
In small intestine, at low concentrations, the process is Primarily in free form or None None Erythrocyte Transketolase Activation
carrier-mediated. At higher concentrations, Bound to albumin as Assess Thiamin Nutritional Status
absorption also occurs via passive diffusion. Thiamine mono- Activation of apo-transkeolase in
phosphate (TMP) erythrocyte lysate by TPP/TDP added in vitro
FUNCTIONS DEFICIENCY
Central role in energy-yielding metabolism especially in carbohydrate WET BERIBERI
metabolism  In areas where polished rise is major component of diet
 TPP serves as coenzyme for three multienzyme complexes  Chronic Peripheral Neuritis
NAME ROLE  Edema
Pyruvate dehydrogenase Catalyze oxidative decarboxylation  Dilated Cardimyopathy
in carbohydrate metabolism  Heart failure
α-ketoglutarate dehydrogenase Catalyze oxidative decarboxylation DRY/SHOSHIN/ACUTE PERNICIOUS FULMINATING BERIBERI
in citric acid cycle  Heart failure
Branched chain keto acid Catalyze oxidative decarboxylation  Metabolic abnormalities
dehydrogenase in leucine, isoleucine & valine  Peripheral neuropathy in legs
metabolism in skeletal muscle WERNICKE-KORSAKOFF SYNDROME
Transketolase Pentose Phosphate pathway in  Primarily in association with chronic alcoholism and impaired absorption
skeletal muscle  Life threatening lactic acidosis
 TTP serves role in nerve conduction; it phosporylates, and activates  Mental confusion
chloride channel in nerve membrane  Gait ataxia
 Nystagmus (to-fro motion of eye balls)
 Opthalmoplegia (weakness of eye muscle)
 Wernicke encephalopathy (memory problems)
 Korsakoff dementia (Hallucinations)
 VITAMIN B2 13
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Riboflavin FMN 1.3 mg 1.1 mg 1.4 mg 1.6 mg Milk Products (yogurt, cheese)
Flavin Mononucleotide (FMN) FAD Enriched or Whole Grains
Falvin adenine dinucleotide (FAD) Meat Products (Chicken, Beef, Fish)
Egg
ABSORPTION TRANSPORT STORAGE TOXICITY STATUS
In proximal parts of small intestine where Flavin As Falvin adenine Erythrocyte Glutathione Reductase
riboflavin is converted to FMN by action of Mononucleotide dinucleotide (FAD) (90%) Activation
flavokinase in presence of ATP FMN and Flavin Mononucleotide None Assess Riboflavin Nutritional Status
Free form of riboflavin is absorbed directly (FMN) (10%) in liver, kidney Activation of a Erythrocyte Glutathione
and heart. Reductase by FAD added in vitro
FUNCTIONS DEFICIENCY
Central role in lipids and carbohydrates metabolism (Mitochondrial Respiratory Chain &Citric Widespread but not fatal as it accompanies other vitamin
acid cycle) diseases
 FMN Dependent Enzymes  Seborrheic Dermatitis (inflammation of skin)
 Carbohydrates Metabolism: Pyruvate/Alpha-ketoglutarate/Succinate  Cheilosis (fissuring at corners of mouth)
dehydrogenase  Glossitis (Tongue appearing smooth and dark)
 Lipid Metabolism: Acyl CoA dehydrogenase
Key enzymes in fatty acid and amino acid oxidation
 FMN Dependent Enzymes
 Protein Metabolism: Glycine Oxidase and D-Amino Acid Oxidase
 Purine Metabolism: Xanthine Oxidase
 FAD Dependent Enzymes
 Protein Metabolism: L-Amino Acid Oxidase
Coenzymes in redox reactions (FAD, FMN) forms FMNH2 or FADH2
Prosthetic group of flavoproteins e.g.
 NADH deydrogenase [FMN]
 Succinate dehydrogenase [FAD]
Being light sensitive, riboflavin is used in phototherapy for hyperbilirubinemia
Because of intense yellow colour, it is used in food additive.
 VITAMIN B3 14
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Niacin Nicotinamide Adenine Dinucleotide 16 mg 14 mg 18 mg 17 mg Internal Sources:
Nicotinic Acid (NAD+) From essential amino acid tryptophan
Nicotinamide (Vitamin B2 Nicotinamide Adenine Dinucleotide External Sources:
& B6 are also required Phosphate (NADP+) Milk and Eggs
for its synthesis from Meat, Chicken, Fish
tryptophan) Liver
Unrefined Whole-Grain and Enriched Breads and Cereals
ABSORPTION & FORMATION TRANSPORT STORAGE TOXICITY
Formation: Transported primarily None While used in treatment of hyperlipidemia (1-6
Synthesized in the body from essential amino acid tryptophan as nicotinamide, & as g/day Niacin)
(1 mg niacin = 60 mg Tryptophan) nicotinic acid  Dilatation of blood vessels
Niacin Food Content  Acute , prostaglandin-mediated flushing
Niacin eq (mg) = Preformed Niacin (mg) + 1/60 Tryptophan (mg)  Skin irritation/itching
Most of niacin in cereals is biologically unavailable Use of Aspirin to inhibit prostaglandin
Absorption: synthesis
NAD & NADP hyrolyzed to free nicotinamide Nicotinic Acid & Nicotinamide (500 mg/day)
Absorbed in small intestine & stomach mostly by passive diffusion  Liver Damage
FUNCTIONS DEFICIENCY
Coenzyme in redox reactions (NAD+ and NADP+ reduced to NADH PELLAGRA
and NADPH respectively) Characterized by the disease involving skin, GIT and CNS
NAD is a source of ADP Ribose Women are more affected (Tryptophan metabolism inhibited by estrogen metabolites)
 ADP-ribosylation of proteins Symptoms (3D + 1D)
 Poly-ADP-ridosylation of nucleoproteins (DNA Repair Mechanism)  Dermatitis (Photosensitive)  Diarrhea  Dementia  Death (if untreated)
Intracelluar Calcium Regulation & Cell Signaling Causes
 In response to Neurotransmitters and Hormones , via cyclic  Corn-based diets (Corn has low niacin & tryptophan content)
ADP-ribose and nicotininc acid adenine dinucleotide formed  Genetic Diseases (despite adequate intake of both tryptophan and niacin)
from NAD  Hartnup Disease: Defect in membrane transport mechanism of tryptophan,
Treatment of Hyperlipidemia Type IIb (VLDL and LDL ) resulting in large loss due to intestinal malabsoprtion and failure of renal
1.5 g/day of Niacin = Inhibit Lipolysis in adipose tissue  FFA Synthesis  reabsorption
 TAG Synthesis (VLDL)   Cholestrol (LDL)   Carcinoid Syndrome: Metastasis of Primary Liver tumour of enterochromaffin cells,
which synthesizes 5-hydroxytryptamine. (60% of tryptophan metabolism defected)
 VITAMIN B5 15
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Pantothenic Acid Coenzyme A (CoA) 5 mg 5 mg 6 mg 7 mg Widely spread in foods
Acyl Carrier Protein Dairy Products (Milk, Yogurt, Cheese)
(ACP) Organ Meats, Beef, Fish
Sunflower Seeds
ABSORPTION TRANSPORT STORAGE TOXICITY
In small intestine, by passive diffusion after hydrolysis of Free Form No No
pantothenic acid to coenzyme A
FUNCTIONS DEFICIENCY
Coenzyme A (CoA) takes part in Not been reported as sources are widely distributed
 Citric Acid Cycle (Succinyl CoA)
 Fatty Acid Oxidation (Fatty Acyl CoA)
 Acetylations (Acetyl CoA)
 Cholesterol Synthesis
 Steroids Synthesis
 Neurotransmitters Synthesis
Acyl Carrier Protein (ACP) takes part in
 Fatty Acid Synthesis (Fatty Acid Synthase)
 VITAMIN B6 16
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
PN Pyridoxine (plants) Pyridoxal 5’- 1.7 mg 1.5 mg 1.9 mg 2 mg Meats, Fish, Poultry
PM Pyridoxamine (animals) phosphate (PLP) Potatoes
PL Pyridoxal (animals) Legumes
PNP Pyridoxine 5’-phosphate Non-citrus Fruits
PMP Pyridoxamine 5’-phosphate Fortified Cereals
PLP Pyridoxal 5’-phosphate Liver
Soy Products
ABSORPTION TRANSPORT STORAGE TOXICITY STATUS
Dephosphorylated to PN, PM, PL and Most PLP transported bound No 100-200 mg/day By assaying activation of
Absorbed by passive diffusion from small to albumin Neurological damage erythrocyte transaminases by PLP
intestine into blood to liver PL, PN, PM & PMP also found added in vitro
Most converted to PLP in liver in blood >500 mg/day Also by plasma concentration
Sensory Neuropathy measurements
FUNCTIONS DEFICIENCY
Coenzyme for many enzymes involved in amino acid metabolism Dietary deficiencies are rare
 Transamination Deficiency in Adults due to Isoniazid
 Deamination  Due to formation of inactive derivative of PLP
 Decarboxylation  Causes abnormalities of tryptophan and methionine
 Condensation metabolism
Cofactor of glycogen phosphorylase (Glycogen Metabolism)  Increased sensitivity to actions of low concentrations of
 80% of body total vitamin B6 is PLP in muscle associated with glycogen phosphorylase steroids (Estrogens, Androgens, Cortisol, Vitamin D)
which is present in starvation to liver and kidney Development of hormone dependent cancer of
Important in steroid hormone action breast, uterus, prostate
 Terminates the action of hormones as PLP removes hormone-receptor complex from Deficiencies in New Borns
DNA binding  Fed Formulas low in B6
May be effective in treating premenstrual syndrome (any of a complex of symptoms including  Alcoholism
emotional tension and fluid retention experienced by some women in the days immediately  Women taking oral contraceptives
before menstruation)
 VITAMIN B7 (H) 17
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Biotin Carboxybiotin 30 μg 30 μg 30 μg 35 μg Internal Sources:
Biocytin Intestinal Bacteria
Carboxybiotin External Sources:
Egg
Fish
Yeast
Avocado
ABSORPTION & FORMATION TRANSPORT STORAGE TOXICITY
Biotindiase removes biotin from food and it is then Free Unbound Form No No
absorbed by passive diffusion/ sodium multivitamin
transporter mechanisms from small intestine into blood
Formed by GIT bacteria
FUNCTIONS DEFICIENCY
Coenzyme in Carboxylation reactions (Transfer CO2) Not been reported as sources are widely distributed and also
 Acetyl CoA carboxylase (Fatty acid synthesis) formed by GIT bacteria
 Pyruvate carboxylase (Gluconeogenisis & Citric Acid Cycle) Addition of raw egg white to diet as a source of of protein can
 Propionyl CoA carboxylase (Metablosim of Amino Acids and Degradation of Odd Chain induce biotin deficiency
Fatty Acids)  Raw egg = AVIDIN glycoprotein
 Methylcrotonyl carboxylase (Metabolism of Leucine)  Avidin binds biotin tightly and prevent its absorption from
 Holocarboxylase synthetase intestine
Regulation of Cell Cycle  20 raw eggs/day with normal diet for a week or 2 = Biotin
 Through its action to biotinylate Key Nuclear Proteins Deficiency
Dermatitis
Hair Loss
Loss of appetite
Nausea
Salmonellosis (infection due to Salmonella enterica)
 VITAMIN B9 (M) 18
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Folic Acid (pteoryl glutamate) Tetrahydro Folic Acid 400 μg 400 μg 600 μg 500 μg Dietary Folate Eq (DFE) = Food Folates (μg) + 1.7 Folic Acid (μg)
(THF) Legumes (Beans, Peas, Lenticels) : 179 μg DFE
Green Leafy Vegetables (Beans, Spinach) : 131 μg DFE
Fortified Foods & Supplements (Sliced Bread) : 84 μg DFE
ABSORPTION TRANSPORT STORAGE TOXICITY
Polyglutamate forms hydrolyzed to monoglutamate form by folate Transported in portal circulation as 5-methyl THF No No
conjugase present in small intestine Also found as a monoglutamate in blood
Absorbed with folate-binding proteins through passive diffusion
Reduced to THF in enterocytes, then metylated to 5-methyl THF or
formylated to 5-formyl THF
FUNCTIONS DEFICIENCY
Reduced, Coenzyme involved actively in one carbon metabolism MEGALOBLASTIC ANEMIA
 Methylation of Deoxyuridine monophosphate (dUMP) to thymidine monophosphate Characterized by deficiency of Vitamin B12 & Folic Acid
(TMP) catalyzed by thymidine synthase (Synthesis of DNA) Vitamin B12 deficiency  Impaired Folic Acid Metabolism 
 N-5,N-10 Methylene THF is reduced to methyl group with release of DHF, which is Functional Folate deficiency  Diminished synthesis of purine
redcued back to THF by DHF reductase nucleotides and TMP  Erythropoiesis disturbed  Accumulation
Binding Position (Pteoryl) Products Role of large immature RBCs precursors (megaloblasts) & hyper-
N-5 N-5 Formyl THF (Folinic acid) segmented neutrophils in bone marrow and blood 
N-5 Formimino THF Megaloblastic Anemia
N-5 Methyl THF Methionine synthesis from Hcy Symptoms:
N-10 N-10 Formyl THF Purine nucleotide syntheisis  Poor absorption due to pathology of small intestine, alcoholism
N-5 and N-5,N-10 Methenyl THF  Treatment with drugs (methotrexate) that are dihydrofolate
N-10 both N-5,N-10 Methylene THF TMP synthesis & Serine synthesis reductase inhibitors

BENEFICIAL EFFECTS OF INHIBITORS AND SUPPLEMENTATIONS

Inhibitors of Folate Metabolism Folic Acid Supplementations
 Anticancer drug (Methotrexate)  Reduce incidence of spina bifida and NTDs (400 μg/day before conception & in 1st Trimester)
(analogue of N-10 Methyl THF)  Reduce hyperhomocycteinemia (Atherosclerosis, thrombosis, hypertension reduced)(Reduce CVD & stroke incidence
 Antibacterial drug (Trimethoprim)  Rectify Megaloblastic Anemia but not the irreversible of vitamin B12 deficiency  Mask Vitamin B12 deficiency (mostly
 Antimalarial drug in elder people with atrophic gastritis)
(Pyrimethamine)  Reduce the incidence of some cancers due to impaired methylation of CpG in DNA (but using anticonvulsants while
in treatment of epilepsy, increases rate of transformation of preneoplastic colorectal polyps into cancers)
FUNCTIONS OF VITAMIN B9 19
 VITAMIN B12 20
Catalogued by Ali Raza Chaudary

ACTIVE RDA
OTHER NAMES DIETARY RESOURCES
FORMS M F P L
Cobalamine (Cobalt Methylcobalamine 2.4 μg 2.4 μg 2.6 μg 2.8 μg Internal Sources:
containing compound (cyanide  methyl) By microorganisms
containing corrin ring) Deoxyadenosyl External Sources: (Not in plants)
Non vitamin corrinoids acts as cobalamine (cyanide Sea food (Shell fish, Fish) : 26 μg/ounce
anti-metabolites for vitamin  deoxyadenosine) Red Meat (Beef, Lamb, Liver) : 1.3 μg/ounce
Chicken : 0.25 μg/ounce
Eggs, Dairy Products, Fortified Cereals
RELEASE & ABSORPTION (by Schilling Test) TRANSPORT STORAGE TOXICITY STATUS
Release from food in acidic environment of stomach B12 Binds to Primarily in liver No B12 deficiency
Free B12 bind to glycoprotein present in saliva (Haptocorrin/ R-protein/ transcobalamin II and then 
Cobalophilin) for transport released to bile Accumulation of
Complex moves into intestine Enterohepatic and efficiently Methylmalonyl CoA
Glycoprotein hydrolyze to release B12 circulation reabsorbed in 
Bind to another glycoprotein (intrinsic factor IF) (only active vitamin B12) ileum Urinary excretion of
Complex travels through intestine methylmalonic acid
Binds cubulin receptor on surface of mucosal cells in ileum 
From here transported to general circulation B12 Status assessed

FUNCTIONS
Coenzyme for isomerization of methylmalonyl CoA by methymalonyl mutase to Succinyl CoA
 Intermediate in catabolism of valine
 Carboxylation of propionyl CoA arising in catabolim of isoleucine, cholesterol and FFA with odd number
 Directly from propionate (major product in microbal fermentation in rumen)
Coenzyme in folic acid metabolism (remethylation of Homocysteine Hcy to Methionine by Methionine synthase)
DEFICIENCY
PERNICIOUS ANEMIA
Causes:
 Severe malabsorption of vitamin B12 due to achlorhydria (reduced gastric acid secretion in elder people)
 Autoimmune destruction of gastric parietal cells i.e. responsible for synthesis of IF or production of anti-IF antibodies
 Pancreatic insufficiency causing excretion of cobalophilin bound B12 instead of absorption
 Partial/Total gastrectomy
 Strict vegetarians as B12 is not found in plants
 Symptoms:
 Anemic Patient
 Neuropsychiatric symptoms
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 Irreversible CNS effects (degeneration of spinal cord)
Treatment:
 Lifelong treatment with high dose of oral B12 or IM injection of cyanocobalamin
FUNCTIONAL FOLATE DEFICIENCY (FOLATE TRAP) to MEGALOBLASTIC ANEMIA
Vitamin B12 deficiency  B12 dependent enzyme absent (methionine synthase)  N-5 Methyl THF utilization or conversion to other THF forms   Impaired
methylation of Hcy to Methionine  Folate trapped in N-5 Methyl THF  Accumulation  Diminished synthesis of purine nucleotides and TMP  Erythropoiesis
disturbed  Accumulation of large immature RBCs precursors (megaloblasts) & hyper- segmented neutrophils in bone marrow and blood  Megaloblastic
Anemia

ABSORPTION OF VITAMIN B12

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