Role of nutritional supplementation in reducing the levels of homocysteine.

Elevated plasma homocysteine level is a risk factor for atherosclerotic disease. Plasma homocysteine levels are influenced by genetic, physiological and lifestyle factors. Among the lifestyle factors, diet plays a significant role. Dietary intakes of folate, vitamins B12, B6 and B2 have been reported to be inversely related to plasma homocysteine concentration. Prevalence of subclinical deficiencies of these vitamins is high in Indian population. Folate status is the major determinant of plasma homocysteine level and there is a strong inverse correlationship between plasma homocysteine level and serum or erythrocyte folate levels. A combination therapy with B vitamins--folate, vitamins B12 and B6 is an effective means to reduce elevated homocysteine levels in general people and in patients with myocardial infarction. To maintain low plasma homocysteine concentration, people should be advised to increase their consumption of pulses, eggs, green leafy vegetables and fruits which are rich in B vitamins.

Fibrinogen and homocysteine levels in coronary artery disease.

Conventional risk factors like high serum cholesterol, smoking and hypertension do not explain all the mortality and morbidity due to coronary artery disease in Indian population. Novel factors like plasma fibrinogen and homocysteine have been currently recognised as independent risk factors for coronary artery disease. A case-control study was carried out to examine the role of plasma fibrinogen, homocysteine, lipid profile and anthropometric parameters in angiographically established coronary artery disease patients. The relationship between the biochemical and anthropometric parameters was also examined. Fifty-eight male patients in the age range of 35-60 years with angiographically established coronary artery disease and equal number of matched-controls were the subjects of this study. Cases with coronary artery disease had significantly higher waist-to-hip ratio, waist-to-thigh ratio, plasma fibrinogen and total cholesterol. Mean plasma total homocysteine levels were not significantly different between cases and controls. In Indian population, elevated plasma fibrinogen and abdominal obesity appear to be significantly associated with coronary artery disease.

Riboflavin metabolism--relevance to human nutrition.

Studies in developing countries like India have revealed a very high incidence of biochemical riboflavin deficiency, particularly in women and children as judged by erythrocyte glutathione reductase activation test (EGR-AC). Riboflavin deficiency can cause conditioned deficiency of vitamin B6 and the mucocutaneous lesions observed in these two vitamins deficiencies could be due to impaired skin collagen maturity. Subclinical riboflavin deficiency impairs psychomotor function and vitamin B2 requirement may be enhanced during increased physical activity. Riboflavin status is not dependent exclusively on dietary intake of the vitamin, certain non-dietary factors can modify riboflavin status. Respiratory infection, certain diseases, drugs and hormones can influence riboflavin metabolism.

Effect of pyridoxine or riboflavin supplementation on plasma homocysteine levels in women with oral lesions.

BACKGROUND: A moderate increase in plasma homocysteine level has been reported to be involved in neural tube defects, which can be prevented with folic acid supplementation. Folic acid, vitamins B6- and B12-dependent enzymes are required to metabolize homocysteine. A study in rats showed higher tissue homocysteine levels in riboflavin as well as pyridoxine deficiency. We studied the effect of treatment with pyridoxine or riboflavin on plasma total homocysteine concentration in women with clinical and biochemical deficiencies of riboflavin and pyridoxine. METHODS: Plasma total homocysteine concentrations were measured in 20 women with glossitis and angular stomatitis before and after supplementation with pyridoxine or riboflavin. RESULTS: Pyridoxine treatment significantly reduced plasma homocysteine concentration while riboflavin treatment did not have a significant effect. CONCLUSIONS: Plasma total homocysteine levels tended to be higher in women with clinical and biochemical deficiency of vitamin B6 and therapy with pyridoxine reduced its level significantly. Riboflavin supplementation did not have a significant impact on plasma homocysteine concentration in women with glossitis and angular stomatitis.

Effect of riboflavin or pyridoxine deficiency on inflammatory response.

Inflammatory response has been assessed in riboflavin or pyridoxine deficient rats. Edema was increased by 54% in pyridoxine deficiency as compared to weight-matched control rats. Food restriction per se reduced the volume of edema by 63%. In pyridoxine deficiency, concentrations of thiobarbituric acid reactive substances (which indicate the extent of lipid peroxidation) increase by 30 and 43% respectively in the edematous tissues of the paw as well as in the wounded skin. Both these parameters were not affected by riboflavin deficiency. Activities of NADPH oxidase and superoxide dismutase in elicited leukocytes from peritoneal cavity were reduced by 54 and 52%, respectively, in riboflavin deficiency but were unaltered in pyridoxine deficiency. Superoxide level and acid phosphatase activity were not influenced by either of the deficiencies, whereas hydrogen peroxide level was increased by 48% in riboflavin deficiency. Food restriction did not affect leukocyte enzymes or the levels of reduced oxygen species. The data suggest that inflammation is enhanced in pyridoxine deficiency but not in riboflavin deficiency.

Mechanism of impaired skin collagen maturity in riboflavin or pyridoxine deficiency.

To elucidate the biochemical basis of impaired skin collagen maturity in pyridoxine-or riboflavin-deficient rats the following two mechanistic possibilities were tested: (i) Reduction in the activity of skin lysyl oxidase (EC 1·4·3·13) which initiates the cross-linking of collagen and (ii) putative rise in homocysteine level leading to neutralization of allysine (α-aminoadipic acid δ-5-semialdehyde)or hydroxyallysine (hydroxy α-aminoadepic acid (δ-semialdehyde) in collagen by the formation of thiazine complexes. Skin lysyl oxidase activity was not affected in pyridoxine deficiency suggesting that pyridoxal phosphate may not be its cofactor. In riboflavin deficiency, lysyl oxidase activity was not altered in the newly regenerated rat skin but a slight reduction was observed in the skin of 18-day-old rat pups. This could be related to the body weight deficit rather than deficiency per se. Aldehyde content of purified salt soluble collagen of regenerated skin was significantly reduced in both the deficiencies. A 2 to 4-fold increase in the concentration of skin homocysteine was observed in both the deficiencies. The results suggest that increase in skin homocysteine level may be responsible for the impaired skin collagen maturity in riboflavin or pyridoxine deficiency.