A. History: This was first isolated by Roger J. Williams in 1938 from yeast and liver concentrates. On account of its wide distribution, he named it as pantothenic acid (pantosG = everywhere). The coenzyme form of this vitamin (coenzyme A or CoA-SH) was isolated and its structure determined by Fritz A. Lipmann. The chemical synthesis of this coenzyme was, however, described by Khorana in 1959. This vitamin is sometimes called as filtrate factor or the yeast factor.
B. Occurrence: Although widespread in nature, yeast, liver and eggs are the richest sources of it. The vegetables (potatoes, sweet potatoes, cabbage, cauliflower, broccoli) and fruits (tomatoes, peanuts) and also the skimmed milk, wheat bran, whole milk and canned salmon are some of the less important sources. In most animal tissues and microorganisms, it occurs as its coenzyme.
C. Structure: Pantothenic acid (C9H17NO5) is an amide of pantoic acid (α, γ-dihydroxy-β, β-dimethyl butyric acid) and β-alanine D. Properties. Pantothenic acid is a pale yellow viscous oil, soluble in water and ethyl acetate but insoluble in chloroform. It is stable to oxidizing and reducing agents but is destroyed by heating in an acidic and alkaline medium (i.e., it is heat-labile).
E. Metabolism: Pantothenic acid can be synthesized by green plants and various microorganisms (Neurospora, Escherichia coli, Bacteria linens) but not by mammals. Hence, this must be present in the diet to serve as a starting point for coenzyme A (CoA). Coenzyme A is richly found in the liver and in poor quantities in the adrenals. There may be as much as 400 mg of CoA per kilo of liver. It functions in acetylation reactions. In order to be effective, CoA must be present in the form of acetyl-CoA. It may arise in many ways but the most common way of its production is that CoA, in the presence of ATP, acetate and a suitable enzyme, is converted into acetyl CoA. The overall reaction may be shown in 3 steps :
B. Occurrence: Although widespread in nature, yeast, liver and eggs are the richest sources of it. The vegetables (potatoes, sweet potatoes, cabbage, cauliflower, broccoli) and fruits (tomatoes, peanuts) and also the skimmed milk, wheat bran, whole milk and canned salmon are some of the less important sources. In most animal tissues and microorganisms, it occurs as its coenzyme.
C. Structure: Pantothenic acid (C9H17NO5) is an amide of pantoic acid (α, γ-dihydroxy-β, β-dimethyl butyric acid) and β-alanine D. Properties. Pantothenic acid is a pale yellow viscous oil, soluble in water and ethyl acetate but insoluble in chloroform. It is stable to oxidizing and reducing agents but is destroyed by heating in an acidic and alkaline medium (i.e., it is heat-labile).
E. Metabolism: Pantothenic acid can be synthesized by green plants and various microorganisms (Neurospora, Escherichia coli, Bacteria linens) but not by mammals. Hence, this must be present in the diet to serve as a starting point for coenzyme A (CoA). Coenzyme A is richly found in the liver and in poor quantities in the adrenals. There may be as much as 400 mg of CoA per kilo of liver. It functions in acetylation reactions. In order to be effective, CoA must be present in the form of acetyl-CoA. It may arise in many ways but the most common way of its production is that CoA, in the presence of ATP, acetate and a suitable enzyme, is converted into acetyl CoA. The overall reaction may be shown in 3 steps :
- ATP + Enzyme ���� ������������ Adenylic acid-Enzyme + Pyrophosphate
- Adenylic acid-Enzyme + CoA ���� ������������ CoA-Enzyme + Adenylic acid
- CoA-Enzyme + Acetate ���� ������������ Acetyl-CoA + Enzyme
The acetyl groups may be transferred to an acetyl acceptor in the presence of a suitable acceptor. This may occur in two ways : either the acetyl group is attached to the accepting groupat the carbonyl end (head reaction) or at the methyl end (tail reaction).The only known metabolic fate of vitamin B3 is its participation in the formation of the biologically important coenzyme A. It functions as a thioester of carboxylic acids.
F. Deficiency: A deficiency of pantothenic acid leads to depigmentation of the hair in rats, pigs and dogs and to depigmentation of feathers in chicks. Atrophy of the adrenal cortex with necrosis and hemorrhage may also occur in animals including rat. Corneal changes consisting of vascularization, thickening and opacity may be seen. In human beings, no definite deficiency syndrome has been ascribed to pantothenic acid, probably because of the ubiquitous nature of this vitamin and because of the fact that a little amount of this vitamin can perhaps be synthesized in the body. Its correlation with achromotrichia (premature greying of the hair) has been described in the case of man, sometimes. But it seems too much to hope that grey hair can be averted by attention to diet ; rather it appears we must expect to go grey in spite of this vitamin.
G. Human requirements: The dietary allowance dose has not been officially worked out. Yet, 5—10 mg per day of vitamin B3 has been suggested.
F. Deficiency: A deficiency of pantothenic acid leads to depigmentation of the hair in rats, pigs and dogs and to depigmentation of feathers in chicks. Atrophy of the adrenal cortex with necrosis and hemorrhage may also occur in animals including rat. Corneal changes consisting of vascularization, thickening and opacity may be seen. In human beings, no definite deficiency syndrome has been ascribed to pantothenic acid, probably because of the ubiquitous nature of this vitamin and because of the fact that a little amount of this vitamin can perhaps be synthesized in the body. Its correlation with achromotrichia (premature greying of the hair) has been described in the case of man, sometimes. But it seems too much to hope that grey hair can be averted by attention to diet ; rather it appears we must expect to go grey in spite of this vitamin.
G. Human requirements: The dietary allowance dose has not been officially worked out. Yet, 5—10 mg per day of vitamin B3 has been suggested.
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