Download Neuroscience-3 Vitamin B6,

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VITAMIN B-6
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Introduction

Vitamin B6 is actually a collective term for three
naturally occurring pyridines that are functionally
and metabolically related:

Pyridoxine

Pyridoxal

Pyridoxamine
Discovered during Nutritional studies on rats in 1930
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Chemical structure
Pyridoxal
Pyridoxine or Pyridoxol
2 Methyl.3 hydroxy,4,5 dihydroxymethyl pyridine
Pyridoxamine
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Active forms are:

Pyridoxal Phosphat

Aldehyde group at position 4 can
reversibly attach with NH3.
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Food sources

Found in wide varieties of foods.

Beans, Legumes and nuts

Eggs,Meats ( beef,chicken breast)

Fish (Trout,Salmon, tuna)

Bread and cereals

Spinach and tomato

Banana
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Functions

Vitamin B6 is involved in variety of metabolic
processes.

Plays a major role in amino acid metabolism
Trasamination
Decarboxylation
Transulfuration
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Functions

Needed for conversion of
Tryptophan to niacin
Formation of melanin
Breakdown of glycogen to glucose

Inter conversion of glycine and serine where it
functions along with Folic Acid.
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Absorption and Metabolism

Readily absorbed from intestine.

In cytoplasm it is converted into Pyridoxal
phosphate and pyradoxalamine Phosphate by
pyridoxal Kinase and ATP.

These are the active forms of the vitamin.

Mainly found in extra-cellular fluid
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
Concentration is relatively high in
 Leukocytes
 Nerve tissues and
 Liver

As water soluble, very little is stored and
Any excess, is excreted in urine in the form of
pyridoxic acid.

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Recommended Daily Allowances

The daily requirements of Vitamin B6
Directly related to protein intake
RDA
 2.2 mg for men and

2 mg for women.
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Effects of Deficiency

After prolong deficiency is commonly seen in
pregnant women and infants.

Dermatitis

Glossitis

Blood disorders
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Dermatitis
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Seborrheic dermatitis
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


Cheilosis
Angular stomatitis
Peripheral neuropathy and
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Toxic Effects
Very limited toxicity in humans
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FOLIC ACID
FOLACIN
Vit.B 10
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STRUTURE
Folic acid is a conjugated molecule consisting of a pteridine ring
structure linked to para-aminobenzoic acid (PABA) that forms
pteroic acid. Folic acid itself is then generated through the
conjugation of glutamic acid residues to pteroic acid
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Folic Acid

positions 7 & 8 carry hydrogens,in Dihydrofolate
(DHF)

positions 5-8 carry hydrogens, in Tetrahydrofolate
(THF)
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
Folacin is generic name for folic acid and
related compounds.

The chemical term for folacin or folic acid
is pteroylglutamic acid.
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Food Sources

The richest sources of folacin include
 Liver
 Spinach
 Wheat
 Yeast and
 Dry beans

Almost all deep green leafy vegetables are also
good sources of this vitamin
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Absorption and Metabolism




Plants Folic Acid contains 7 or 5 Glutamyl
Residues linked together by a peptide bond.
The peptide bond is hydrolyzed by intestinal
enzymes and the compound with one glutamyl
residues is formed
Folic acid in the form of its monoglutamyl form is
absorbed only.
Then it is reduced to tetrahydrofolate in the
intestinal mucosa during absorption.
Vitamin C is required for this reduction
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
All forms of folacin are equally utilized in the body

More folacin is excreted in urine and feces than is
accounted for in the diet, which indicates that this
vitamin is also synthesized by intestinal flora

Most of folacin is stored in liver

Folic acid is converted to its biologically active
form folinic acid in the liver
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Recommended dietary allowance

RDA for adults in 400 g of folacin daily
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Deficiency Diseases

Folate deficiency results in complications nearly
identical to those of vitamin B12 deficiency.

The most pronounced effect of folate deficiency on
cellular processes is upon DNA synthesis.

The result is megaloblastic anemia as for vitamin
B12 deficiency.
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Megaloblastic anemia
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Deficiency Diseases

The inability to synthesize DNA during erythrocyte
maturation leads to abnormally large erythrocytes
termed macrocytic anemia.

Folate deficiencies are rare due to the adequate
presence of folate in food.

Poor dietary habits as those of chronic alcoholics
can lead to folate deficiency.
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Deficiency Diseases

The predominant causes of folate deficiency in
non-alcoholics are impaired absorption or
metabolism or an increased demand for the
vitamin.

Certain drugs such as anticonvulsants and oral
contraceptives can impair the absorption of folate.

Anticonvulsants also increase the rate of folate
metabolism.
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Deficiency Diseases

Folic acid appears to reduce the risk of stroke

Low blood levels of folic acid are associated with
increased risk of cancer. (Breast, pancreas and
colon)
Damage to DNA caused by folate deficiency may
be the reason.

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Prevention of Neural Tube Defect leading to spina
bifida at the very early stage of pregnancy
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INCREASED REQUIREMENT

The predominant condition requiring an increase
in the daily intake of folate is, pregnancy.

pregnancy and infancy are both characterized by
increased number of rapidly proliferating cells
present in the blood.

The need for folate will nearly double by the third
trimester of pregnancy.
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Possible Toxic Effect

Risk from Folic acid Toxicity is very low.

Tolerable upper intake level for adult is 1 mg/day.

Upper intake level is 800 ug/day for pregnant and
lactating women if less than 18 years of age.

Supplemental level should not increase than the
upper level to prevent folic acid from masking
symptoms of Vitamin B-12
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Vitamin B12
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Introduction

Vitamin B12 includes a group of cobalt, containing
compounds known as cobalamins.
The major forms found in plasma and tissue include

Methyl cobalamin

Adenolylcobalmin and

Hydroxycobalamin.
All of these forms are biologically active.
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Food sources

Vitamin B12 occurs only in animal sources.
The richest sources include

Lamb and beef kidney

Lamb and calf beef

Liver and brain.

Other good sources include

Heart, egg yolk and variety of sea
foods
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Stability and solubility

Stable to heat in aq.medium

Only slightly soluble in water

It is destroyed by strong acid and Alkalies

Little lost during cooking
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Functions

Vitamin B12 is required by all cells of the body,
especially
 Gastro-intestinal tract
 Bone marrow and
 Nervous system.

Within bone marrow, it is involved in conversion of
ribose nucleotides into deoxyribose nucleotides
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Functions (Contd.)

An essential step in DNA synthesis.

If DNA is not synthesized in enough quantities,
large RBC’s (macrocytes) are released into the
blood.
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Absorption and Metabolism

Vitamin B12 is absorbed through receptor sites in
the ileum, mediated by intrinsic factor which is
produced by glands in stomach.

Vitamin is then transported across the intestinal
cell and then into blood stream.

Vitamin B12 is normally stored in liver for 3 to 5
years.
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Recommended Dietary Allowances

The RDA of 3.0 g of Vitamin B12 for adults allows
for maintenance of adequate nutrition and
substantial reserve body pool.
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Effects of Deficiency

Deficiency of Vitamin B12 is usually caused by
defect in absorption rather than by dietary factors

When intrinsic factor is not produced, Vit B12 is not
absorbed.
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Effects of Deficiency (Contd.)

As a result, bone marrow cannot produced mature
red blood cells and so releases the large,
immature precursor (macrocytes) into blood
stream instead.

The symptoms of megalotblastic anemia include
pallor, weight loss, anorexia, glossitis, sprue and
in advanced stages, degeneration of spinal cord.
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Toxic Effect

No toxic effect in humans
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