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Vitamin C 120905

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0% found this document useful (0 votes)
14 views12 pages

Vitamin C 120905

Uploaded by

athulyarenju05
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Ascorbic Acid (Vitamin C)

Vitamin C; Structure.
Biosynthesis of Ascorbic Acid in Animals

Most animals and plants can synthesize ascorbic acid from


glucose. Man, higher primates, guinea pigs and bats are the
only species which cannot synthesize ascorbic acid. They lack
the genes responsible for the synthesis of this enzyme. The
vitamin therefore should be supplied in the diet of these
species.
Biochemical Functions of Vitamin C
1. Hydroxylation of proline and lysine: Hydroxyproline and
hydroxylysine are essential for the formation of cross links in the
collagen, which give the tensile strength to the fibers.
2. Tryptophan metabolism: hydroxylation of tryptophan to 5-hydroxy
tryptophan, for synthesis of serotonin.
3. Tyrosine metabolism: para-hydroxy phenylpyruvate to homogentisic
acid.
4. Iron metabolism: Ascorbic acid reduces ferric iron to ferrous state.
5. Hemoglobin metabolism: Reconversion of met-hemoglobin to
hemoglobin.
Biochemical Functions of Vitamin C

6. Folic acid metabolism: Helps the enzyme folate reductase.


7. Steroid synthesis: Vitamin C helps in the synthesis of bile acids
from cholesterol. The initial 7 alpha-hydroxylase step is
stimulated by the vitamin.
8. Phagocytosis: Ascorbic acid stimulates phagocytic action of
leukocytes.
9. Antioxidant property: Aniline dyes are known to induce bladder
cancer in factory workers. Daily intake of vitamin C reduces this
risk for cancer.
Deficiency Manifestations of Vitamin C
Scurvy
Gross deficiency of vitamin C results in scurvy. Deficiency
in children is named as infantile scurvy or Barlow’s disease.

Hemorrhagic Tendency

In ascorbic acid deficiency, collagen is abnormal and the intercellular


cement substance is brittle. So, capillaries are fragile, leading to the
tendency to bleed even under minor pressure. Subcutaneous hemorrhage
may be manifested as petechia in mild deficiency and as ecchymosis or
even hematoma in severe conditions.

Internal Hemorrhage

In severe cases, hemorrhage may occur in the conjunctiva and retina.


Internal bleeding may be seen as epistaxis, hematuria or melena.
Deficiency Manifestations of Vitamin C
Oral Cavity
In severe cases of scurvy, the gum becomes painful, swollen, and
spongy.
The pulp is separated from the dentine and finally teeth are lost. Wound
healing may be delayed.
Bones
In the bones, the deficiency results in the failure of the osteoblasts to form
the intercellular substance, osteoid. The deposition of bone is arrested. The
resulting scorbutic bone is weak and fractures easily. There may be
hemorrhage into joint cavities. Painful swelling of joints may prevent
locomotion of the patient.
Nails
Spoon-shaped nails are characterized by their concave shape.
Anemia
In vitamin C deficiency, microcytic, hypochromic anemia is seen. Poikilocytosis
and anisocytosis are also common in anemia due to deficiency of vitamin C.

Gingivitis and bleeding gum in


Spoon-shaped nails with red spots in the
Vitamin C deficiency.
nail bed, known as splinter hemorrhage.
Dietary Sources of Vitamin C
Rich sources are amla (Indian gooseberry), guava, lime,
lemon and green leafy vegetables.

Requirement of Vitamin C

Adults - 75 mg/day (equal to 50 mL orange juice).

Pregnancy & lactation - 100 mg/day.

Therapeutic Use of Vitamin C

Vitamin C is used as an adjuvant in infections. Beneficial effect of ascorbic


acid is reported in the treatment of tuberculosis. Clinical dose is 500
mg/day.

Because of its power to heal wounds, vitamin C has been


recommended for treatment of ulcer, trauma, and burns.
Name Coenzyme form RDA Main reaction using Deficiency
the coenzyme disease

Thiamine Thiamine 1–1.5 mg Oxidative decarboxy- Beriberi


pyrophosphate lation of alpha
(TPP) keto acids

Riboflavin Flavin adenine 1.5 mg Dehydrogenation, Glossitis,


dinucleotide oxidised in ETC angular
(FAD) (1.5 ATP) stomatitis
Niacin NAD and NADP 20 mg Dehydrogenation, Pellagra
oxidised in ETC (2.5
ATP)
Pyridoxine Pyridoxal 1–2 mg Transamination, Seizures,
phosphate (PLP) decarboxylation of homocysti-
amino acids nuria
Name Coenzyme form RDA Main reaction using Deficiency
the coenzyme disease
Pantothenic Coenzyme A, 10 mg CoA derivatives, acyl Burning foot
acid ACP carrier proteins syndrome

Biotin Biotin 30-40µg Carboxylation No specific


disease
Folic acid Tetrahydrofolic 200 µg One-carbon group Macrocytic
acid (THFA) carrier anemia
Vitamin Adenosyl B12, 1–2 µg Isomerisation of Megaloblastic
B12 methylcobalamin methylmalonyl-CoA, anemia, Sub-
remethylation of acute
homocysteine to met combined
degeneration
Ascorbic No specific form 75 mg Antioxidant property Scurvy
acid

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