Introduction to vitamins, Different water soluble vitamins

1. Water Soluble
Vitamins
Dr Ifat Ara Begum
Associate Professor
Dept of Biochemistry
Dhaka Medical College
Dhaka
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2. Organic
nutrients
Have no energy
value , not
structural
component of
tissues
Essential
nutrient
Vitamins
Are required in small amount for different
biochemical reactions to support
normal growth, maintenance &
reproduction

3. Sources of vitamins
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Exogenous
source:
Diet Endogenous source:
i. Intestinal flora :
Vitamin K, B12, Biotin
ii. Steroid precursor in
skin: Vitamin D
iii. Tryptophan (AA):
Niacin

4. - Maintains optimum health
- Prevents acute deficiency
disorders
Intermediary metabolism &
energy release
Prophylactic use to prevent
chronic diseases Antioxidant function
Functions of
Vitamins

5. Classification of vitamins
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Fat soluble vitamins
 Hydrophobic, soluble in
fat solvent
 Intestinal absorption
depends on fat absorption
 LP / specific protein is
needed for transport in
blood
 Not readily excreted in
urine
 Storage : Significant, in
Liver & adipose tissues
 Regular dietary supply :
Not needed
 Toxicity: Common
 Only vitamin K has
coenzyme activity
Water soluble vitamins
 Hydrophilic, soluble in water
 Intestinal absorption doesn’t
depend on fat absorption
 No need of LP/ specific
protein for transport in blood
 Readily excreted in urine
 Storage : Limited except for
vitamin B12 & folic acid (in
liver)
Regular dietary supply :
Needed
 Toxicity: Rare
 Coenzyme activity: Common

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Vitamin Chemical name Active / Functional /
Coenzyme form
B1 Thiamine Thiamine pyrophosphate
(TPP)
B2 Riboflavin FAD (Flavin adenine
dinucleotide), FMN
B3 Niacin/ Nicotinic
acid/ Nicotinamide
NAD (Nicotinamide adenine
dinucleotide), NADP
B5 Pantothenic acid Coenzyme A (CoA-SH), Acyl
carrier protein (ACP)
B6 Pyridoxine Pyridoxal phosphate (PLP)
B7 Biotin Biotin
B9 Folic acid / Folate Tetrahydrofolate (FH4)
B12 Cobalamin Methyl cobalamin,
5’-Deoxy adenosyl
cobalamin

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These vitamins are chemically
not related to one another.
They are grouped together,
because,
all of them function in the cells
as coenzymes.

10. Classification
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Energy
releasing
vitamins:
Vitamin B1, B2, B3,
B5 , B7 (Biotin)
Hematopoietic
vitamins:
Vitamin B9
(Folic acid), B12
Others:
Vitamin B6

11. Sources of vitamin B complex
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Endogenous
source:
Niacin, Biotin,
vitamin B12,
Exogenous source:
 Animal sources:
Egg, meat, fish, liver,
milk & milk products
 Plant sources:
Whole grain cereals,
green leafy
vegetables, legumes,
peas, nuts, beans
Vit.
B12 has
no plant
source

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Functions of
Vitamin B
Complex

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B1 /
Thiamine
(TPP)
In glucose oxidation:
a. In oxidative decarboxylation reaction:
 PDH: Pyruvate to Acetyl CoA & CO2
 α-KGDH: α-KG to Succinyl CoA (in TCA
cycle)
b. For Transketolase enzyme of HMP shunt
Helps to
- maintain nerve conduction
&
- functioning of nervous system

14. Remember
 Oxidative decarboxylation of pyruvate and α-KG have
key role in energy metabolism.
So, in thiamine deficiency, ATP production is decreased
with impaired cellular functions.
As glucose is the only fuel for neurons & as optimum
thiamine is specifically important for glucose oxidation,
the deficiency of thiamine will affect the activity of
nervous system.
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15.  Impaired oxidation of pyruvate to acetyl CoA forces the
pyruvate to be converted to lactate.
This lactate acts as vasodilator leading to increased venous
return, high output heart failure and edema.
 Thiamine is useful in the treatment of beriberi, alcoholic
polyneuritis, neuritis of pregnancy /old age.
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B2 /
Riboflavin
(FMN,
FAD)
Concerned with energy metabolism
Coenzyme in oxidation – reduction process /
dehydrogenation process:
e.g.
- Oxidation of succinate to fumarate
- Oxidation of fatty acyl CoA to α, β fatty acyl
CoA

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B3 / Niacin
(NAD,
NADP)
Same as Riboflavin
e.g.
- Oxidation of malate to oxaloacetate
- Oxidation of pyruvate to acetyl CoA etc
B5 /
Pantothenic
acid
(CoA-SH)
Formation of :
i) Active acetate (acetyl CoA):
 For synthesis of FA, Ketone bodies,
cholesterol etc
 Oxidizes in TCA cycle
ii) Active succinate (succinyl CoA):
 For synthesis of heme
 ketolysis
Helps in fatty acid oxidation

18. Therapeutic use of vit.B3
In the reduction of:
- Plasma LDL-C
- Plasma TAG
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B6 /
Pyridoxine
(PLP)
Coenzyme for transamination &
deamination of amino acids (Main
function)
Coenzyme of phosphorylase during
Glycogenolysis:
Decarboxylation of :
 Histidine : to produce histamine
 Glutamate: to produce GABA
Synthesis of :
 Porphyrin & heme
 Catecholamine
 Serotonin

20. Causes of deficiency of vit. B6
 Treatment of TB with Isoniazid (INH): Common cause
 Rare causes:
Newborn infant fed with infant formula, women taking OCP,
Alcoholics.
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21. Link of INH with vit. B6 deficiency
 INH forms an inactive derivative with Pyridoxal
phosphate.
So, it is recommended to prescribe B6 rich diet during
treatment with INH
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B7 / Biotin
(Biotin)
Coenzyme of carboxylase (to catalyze
carboxylation reaction)
e.g.
- Pyruvate to oxaloacetate
- Acetyl CoA to Malonyl CoA

23. Biotin Antagonist
Avidin (protein present in egg white) :
It tightly binds with biotin hampering absorption of biotin.
So, addition of raw egg white in diet may cause biotin
deficiency
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B9 / Folic
acid
(FH4)
Acts as a carrier of 1-C units (CH3, CH2
group etc) from different amino acids to
use them for synthesis of :
 Purines
 Pyrimidines (dTMP)
 DNA, RNA
 Methionine etc
Helps in neural tube development in early
fetal life

25. Storage of Folic acid
 In liver to some extent
 Total body store is 12-15 mg
 This amount can support body demand for 4-6 months
after stoppage of folic acid intake.
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B12 /
Cobalamin
(Methyl
cobalamin,
5’-Deoxy
adenosyl
cobalamin)
[Synonym:
Extrinsic
factor of
castle
Antipernicio
us anemia
factor]
Interconversion of homocysteine &
methionine reaction: This reaction helps to
 maintain methionine store
&
 ensure availability of FH4 & FH4
subsequently participates in purine, dTMP &
NA synthesis
Conversion of propionyl CoA to succinyl
CoA : Succinyl Co A enters TCA cycle
Maintains Myelin sheath & Epithelial cells
Hemopoiesis by ensuring availability of
FH4

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29. Functional types of vit. B12
 Cyanocobalamin: This is the commercial form.
 Methyl cobalamin: It is the main circulating form.
 5’-deoxy adenosyl cobalamin: It is the main storage form.
 Hydroxy cobalamin: Injectable preparations are in this
form.
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30. Absorption & transport of vit. B12
 Requires Intrinsic Factor for absorption
 Is transported in blood with a protein called
transcobalamin.
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31. Storage of vit. B12
 Stored in liver ,
 Total body store: 4-5 mg
 Stored vitamin B12 is not depleted until 5-6 years after
cessation of intake or absorption
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Deficiency of
Vitamin B
Complex

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Vitamin Deficiency
B1 / Thiamine  Wet beriberi / Cardiac beriberi: Heart
failure , edema
 Dry Beriberi / Neurological beriberi:
Peripheral neuropathy
 Wernicke's encephalopathy : Affects
CNS
 Korsakoff’s psychosis with memory
loss: : Affects CNS
B2 / Riboflavin  Cheilosis: Chapped & fissured lips
 Angular stomatitis: Inflammation of
corner of mouth
 Glossitis
 Seborrheic dermatitis

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Vitamin Deficiency
B3 / Niacin Pellagra , featured by 3 ‘D’
 Dermatitis
 Diarrhoea
 Dementia
B5 /
Pantothenic
acid
 Peripheral nerve damage
 Burning feet syndrome
 Staggering gait
B6 / Pyridoxine  Peripheral neuropathy: Due to lack of
serotonin, GABA, Catecholamine
 Anemia: Due to lack of heme synthesis
 Disorders of AA metabolism

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Vitamin Deficiency
B7 / Biotin  Dermatitis
 Glossitis
 Nausea, anorexia
 Impairment of carbohydrate & fat
metabolism
B9 / Folic
acid
 Megaloblastic anemia : Failure of rapid
DNA synthesis
 Growth failure
 GIT disturbances
 NTDs in fetus during pregnancy like spina
bifida, anencephaly etc
 Hyperhomocysteinemia

37. Causes of Folate deficiency
 Increased physiological demand of folic acid
 Lack of dietary intake
 Malabsorption
 Blood loss
 Drugs
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Vitamin Deficiency
B12/
Cobalamin
 Megaloblastic anemia:
Happens due to 2ndary deficit of FH4 as a
result of folate trap
 Neurological disorders:
Due to irreversible & progressive
demyelination.
e.g.
 Sub acute combined degeneration of
spinal cord
 Peripheral neuropathy
 Dementia
 Optic atrophy
 Hyperhomocysteinemia & atherosclerosis:
Homocysteine level in blood is related with
MI.

39. Folate trap
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40. Megaloblastic Anemia
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Megaloblastic
anemia
Pernicious
anemia
Macrocytic anemia Type of megaloblastic
anemia
Cause:
Folate deficiency,
Vitamin B12 deficiency
Cause:
Deficiency of IF
(As a result, vitamin B12
deficiency secondary to
malabsorption of vitamin
B12 occurs)

42. Causes of IF deficiency
 Autoimmune disease of gastric parietal cells or
 Formation of anti-IF antibodies
 Total / partial gastrectomy
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Chemistry Source Function
Derivatives
of hexose
A reducing
agent
(Benedict’s
test will be
positive )
Citrus fruits
Green chili &
green leafy
vegetables
 Post-translational
maturation of collagen:
Done by hydroxylation of
proline & lysine residues
of collagen
 Enhances absorption of
iron
 Reduces serum
cholesterol concentration
Acts as anti-oxidant
Helps in synthesis of
Catecholamine & Steroid
hormone

45. Therapeutic use of vit. C
Recommended for treatment of:
 Ulcer
 Trauma
 Burns.
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Clinical manifestation of
vitamin C deficiency:
Scurvy
(Caused by defective collagen
synthesis following vitamin C
deficiency)

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 Swollen, spongy and
bleeding gums
 Loosened teeth
 Fragile blood vessels
 Bleeding under the skin
and in deep tissues
 Cutaneous bleeding
leading to woody leg due to
capillary hemorrhage
 Spontaneous bruising
 Joint : Swollen, hemorrhage
 Epistaxis
 Hemorrhage in GIT
 Slow wound healing
 Anemia (iron deficiency anemia)

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When life gives you scurvy, make
lemonade 
SAY “NO” TO SCURVY 

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