A. History: Vitamin B5 refers to nicotinic acid and was named as pellagra
preventive (PP) factor by an Austrian-American physician of the U. S. Public Health Service, Joseph Goldberger (ca 1920) because of its curing action on pellagra (After Goldberger's death, vitamin B5 was sometimes called vitamin G in his honour). The vitamin role on nicotinic acid was first recognized by Conrad Elvehjem and D. Wayne Woolley of Wisconsin University in 1937. As this vitamin has a curing action against blacktongue disease in dogs, it is also called as antiblacktongue factor. It was first isolated by Funk in 1911. Because the name `nicotinic acid' might mislead some people into thinking that tobacco is nutritious, nicotinic acid has been given the alternative official name niacin for public use.
B. Occurrence: Nicotinic acid is widely distributed in nature in plant and animal tissues mainly as its amide called nicotinamide (commercially called niacinamide, to avoid any misassociation with the alkaloid nicotine of tobacco). As dietary tryptophan can be converted, in restricted quantities, to niacin in the body, it can partially substitute for niacin, although other sources of vitamin B5 are necessary. Niacin is most abundantly found in yeast. Liver, lean pork, salmon, poultry and red meat are also good sources, but most cereals contain only small amounts of it. Most vegetables and fruits are poor sources of it. Milk and eggs, which contain very little or practically no niacin, are good pellagra-preventive foods because of their high content of tryptophan. Since a number of stable vegetable articles of diet are not particularly rich in nicotinamide, the vegetarian’s diet may be lacking in this vitamin. Nicotinamide, is present as a constituent in two pyridine nucleotide coenzymes namely NAD and NADP (previously called as DPN and TPN respectively). Since niacin is stable to heating and oxidation, there are only small losses in cooking. Like thiamine, most of vitamin B5 is lost in the milling process.
C. Structure: Niacin (C6H5O2N) is simplest of all the known vitamins. It is a pyridine derivative.
D. Properties: Niacin is a white crystalline substance. It is soluble in ethyl alcohol but is less
soluble in ether and benzene than nicotinamide. It is heat-stable. Nicotinamide, when pure, occurs
as white needle like crystals. It is soluble in water and is stable in air and heat.
E. Metabolism: The conversion of niacin to niacinamide takes place in the kidney and brain slices and also in the liver slices, if glutathione is present. Nicotinamide is synthesized by amidation of nicotinic acid adenine dinucleotide and subsequent degradation of NAD thus formed.
The niacin in man and other animals is derived from the amino acid tryptophan, which also cures pellagra. The conversion of tryptophan to nicotinic acid in the body takes place through a series of intermediate steps,
which are represented below :
Tryptophan → Kynurenine → 3-hydroxykynurenine 3-hydroxyanthranilic acid → ... → Quinolinic acid → Nicotinic acid:
Nicotinamide undergoes methylation in mammalian liver to produce N′-methyl nicotinamide which is oxidized to give corresponding 6-pyridone. In many plant seeds nicotinic acid is, however, converted to trigonelline. The nicotinic acid and its amide both are necessary for the growth of various microorganisms. Pyridine-3-sulfonic acid and its amide both prevent such growth which can be resumed by the addition of these vitamins. The relationship of these growth inhibitors to the two vitamins is not much different with the relationship of p-aminobenzoic acid to sulfanilamide .
The two coenzyme forms of this vitamin, NAD and NADP, carry out 2 important functions in the tissues:
(a) Oxidation of alcohols, aldehydes, amino acids and hydroxy-carboxylic acids.
(b) Reduction of the flavin coenzymes.
F. Deficiency: A deficiency of niacin causes pellagra in man and blacktongue in dogs. Pellagra (of Italian origin, pellis = skin; agra = rough) is characterized by 3 “Ds”, namely dermatitis of the exposed parts, diarrhea and dementia. The early symptoms of pellagra are vague. Anorexia, lassitude, fatigue, burning sensations, numbness and dizziness may be prodromal symptoms. Their manifestation in children who have parasites or chronic disorders may be particularly severe. The most characteristic manifestations are the cutaneous ones, which may develop abruptly or insidiously and may be elicitated by irritants, esp., by intense light. They first appear as symmetric erythema of the exposed surfaces that may resemble sunburn. The lesions are usually sharply demarcated from the healthy skin around them, and their distribution may change very often. The lesions on the hands sometimes have the appearance of a glove (pellagrous glove), and similar demarcations are sometimes seen on the foot and leg (pellagrous boot) or around the neck (Casal necklace). The healed parts of the skin may remain pigmented. The cutaneous lesions are sometimes preceded by stomatitis, glossitis, vomiting or diarrhea. Swelling and redness of the tip of the tongue and its lateral margins may be followed by intense redness of the entire tongue and of the papillae and even ulceration. Nervous symptoms include depression, disorientation, insomnia and delirium. The histologic changes in the nervous system occur relatively late in the disease and consist of patchy areas of demyelinization and degeneration of ganglion cells.
The classic symptoms of pellagra are usually not pronounced in infants and children. Anorexia, irritability, anxiety and apathy are common in “pellagra families”. They may also have sore tongues and lips and the skin is usually dry and scaly. Diarrhea and constipation may alternate and a moderate secondary anemia may occur. Pellagral children often have symptoms characteristic of other nutritional deficiency diseases. As coffee (Coffea arabica) is particularly rich in niacin, the heavy coffee drinkers usually do not develop pellagra. Other factors like thiamine-deficiency also seem to be responsible for this disease. Incredible as it may seem, over 600 deaths were attributed to pellagra in 1948. Pellagra is greatly aggravated in persons kept on a corn diet (as natives of Africa) because corn is very much deficient of tryptophan.
The canine blacktongue disease leads to complete loss of appetite. The inner surfaces of the lips and cheeks develop pustules ; the pustules may also develop on the thorax and abdomen. Intensive salivation and bloody diarrhea are other symptoms.
G. Human requirements: The recommended daily allowance of nicotinic acid is between 8 and 15 mg for children, between 15 and 20 mg for men and between 13 and 15 mg for women. Pregnant and lactating mothers may require up to 20 mg daily.
H. Treatment : Children respond quickly to antipellagral therapy. A well-balanced diet should be augmented with 50-300 mg/day of niacin; 100 mg may be given intravenously in acute cases or in cases of poor intestinal absorption. The diet should be supplemented with other vitamins, especially with other members of B complex group. Sun exposure should be avoided during the active phase; the skin lesions may be covered by applying soothers. The diet of the cured pellagrin should be supervised continuously to prevent recurrence.
preventive (PP) factor by an Austrian-American physician of the U. S. Public Health Service, Joseph Goldberger (ca 1920) because of its curing action on pellagra (After Goldberger's death, vitamin B5 was sometimes called vitamin G in his honour). The vitamin role on nicotinic acid was first recognized by Conrad Elvehjem and D. Wayne Woolley of Wisconsin University in 1937. As this vitamin has a curing action against blacktongue disease in dogs, it is also called as antiblacktongue factor. It was first isolated by Funk in 1911. Because the name `nicotinic acid' might mislead some people into thinking that tobacco is nutritious, nicotinic acid has been given the alternative official name niacin for public use.B. Occurrence: Nicotinic acid is widely distributed in nature in plant and animal tissues mainly as its amide called nicotinamide (commercially called niacinamide, to avoid any misassociation with the alkaloid nicotine of tobacco). As dietary tryptophan can be converted, in restricted quantities, to niacin in the body, it can partially substitute for niacin, although other sources of vitamin B5 are necessary. Niacin is most abundantly found in yeast. Liver, lean pork, salmon, poultry and red meat are also good sources, but most cereals contain only small amounts of it. Most vegetables and fruits are poor sources of it. Milk and eggs, which contain very little or practically no niacin, are good pellagra-preventive foods because of their high content of tryptophan. Since a number of stable vegetable articles of diet are not particularly rich in nicotinamide, the vegetarian’s diet may be lacking in this vitamin. Nicotinamide, is present as a constituent in two pyridine nucleotide coenzymes namely NAD and NADP (previously called as DPN and TPN respectively). Since niacin is stable to heating and oxidation, there are only small losses in cooking. Like thiamine, most of vitamin B5 is lost in the milling process.
C. Structure: Niacin (C6H5O2N) is simplest of all the known vitamins. It is a pyridine derivative.
D. Properties: Niacin is a white crystalline substance. It is soluble in ethyl alcohol but is less
soluble in ether and benzene than nicotinamide. It is heat-stable. Nicotinamide, when pure, occurs
as white needle like crystals. It is soluble in water and is stable in air and heat.
E. Metabolism: The conversion of niacin to niacinamide takes place in the kidney and brain slices and also in the liver slices, if glutathione is present. Nicotinamide is synthesized by amidation of nicotinic acid adenine dinucleotide and subsequent degradation of NAD thus formed.
The niacin in man and other animals is derived from the amino acid tryptophan, which also cures pellagra. The conversion of tryptophan to nicotinic acid in the body takes place through a series of intermediate steps,
which are represented below :
Tryptophan → Kynurenine → 3-hydroxykynurenine 3-hydroxyanthranilic acid → ... → Quinolinic acid → Nicotinic acid:
Nicotinamide undergoes methylation in mammalian liver to produce N′-methyl nicotinamide which is oxidized to give corresponding 6-pyridone. In many plant seeds nicotinic acid is, however, converted to trigonelline. The nicotinic acid and its amide both are necessary for the growth of various microorganisms. Pyridine-3-sulfonic acid and its amide both prevent such growth which can be resumed by the addition of these vitamins. The relationship of these growth inhibitors to the two vitamins is not much different with the relationship of p-aminobenzoic acid to sulfanilamide .The two coenzyme forms of this vitamin, NAD and NADP, carry out 2 important functions in the tissues:
(a) Oxidation of alcohols, aldehydes, amino acids and hydroxy-carboxylic acids.
(b) Reduction of the flavin coenzymes.
F. Deficiency: A deficiency of niacin causes pellagra in man and blacktongue in dogs. Pellagra (of Italian origin, pellis = skin; agra = rough) is characterized by 3 “Ds”, namely dermatitis of the exposed parts, diarrhea and dementia. The early symptoms of pellagra are vague. Anorexia, lassitude, fatigue, burning sensations, numbness and dizziness may be prodromal symptoms. Their manifestation in children who have parasites or chronic disorders may be particularly severe. The most characteristic manifestations are the cutaneous ones, which may develop abruptly or insidiously and may be elicitated by irritants, esp., by intense light. They first appear as symmetric erythema of the exposed surfaces that may resemble sunburn. The lesions are usually sharply demarcated from the healthy skin around them, and their distribution may change very often. The lesions on the hands sometimes have the appearance of a glove (pellagrous glove), and similar demarcations are sometimes seen on the foot and leg (pellagrous boot) or around the neck (Casal necklace). The healed parts of the skin may remain pigmented. The cutaneous lesions are sometimes preceded by stomatitis, glossitis, vomiting or diarrhea. Swelling and redness of the tip of the tongue and its lateral margins may be followed by intense redness of the entire tongue and of the papillae and even ulceration. Nervous symptoms include depression, disorientation, insomnia and delirium. The histologic changes in the nervous system occur relatively late in the disease and consist of patchy areas of demyelinization and degeneration of ganglion cells.
The classic symptoms of pellagra are usually not pronounced in infants and children. Anorexia, irritability, anxiety and apathy are common in “pellagra families”. They may also have sore tongues and lips and the skin is usually dry and scaly. Diarrhea and constipation may alternate and a moderate secondary anemia may occur. Pellagral children often have symptoms characteristic of other nutritional deficiency diseases. As coffee (Coffea arabica) is particularly rich in niacin, the heavy coffee drinkers usually do not develop pellagra. Other factors like thiamine-deficiency also seem to be responsible for this disease. Incredible as it may seem, over 600 deaths were attributed to pellagra in 1948. Pellagra is greatly aggravated in persons kept on a corn diet (as natives of Africa) because corn is very much deficient of tryptophan.
The canine blacktongue disease leads to complete loss of appetite. The inner surfaces of the lips and cheeks develop pustules ; the pustules may also develop on the thorax and abdomen. Intensive salivation and bloody diarrhea are other symptoms.
G. Human requirements: The recommended daily allowance of nicotinic acid is between 8 and 15 mg for children, between 15 and 20 mg for men and between 13 and 15 mg for women. Pregnant and lactating mothers may require up to 20 mg daily.
H. Treatment : Children respond quickly to antipellagral therapy. A well-balanced diet should be augmented with 50-300 mg/day of niacin; 100 mg may be given intravenously in acute cases or in cases of poor intestinal absorption. The diet should be supplemented with other vitamins, especially with other members of B complex group. Sun exposure should be avoided during the active phase; the skin lesions may be covered by applying soothers. The diet of the cured pellagrin should be supervised continuously to prevent recurrence.
0 comments:
Post a Comment