Soluble dietary fibers have been shown to reduce total plasma cholesterol and LDL-cholesterol, the two important risk factors for coronary heart disease. Multiple mechanisms appear to be involved in the hypocholesterolemic response, and data indicate that the profile of operating mechanisms may vary considerably among different dietary fiber sources. The mechanisms which have been suggested include binding of bile acids and interference with their enterohepatic circulation, interference with micelle formation, and reduced hepatic cholesterol synthesis. An examination of hypocholesterolemic action of dietary pectin indicates that this effect is due to a shift of cholesterol from plasma to the hepatic pools.
Hypochlorous acid (HOCl) produced by myeloperoxidase reacts with ammonia to form highly toxic ammonia-chloramine (NH2Cl) in vivo. We examined the abilities of various amino acids to compete with ammonia to form only mildly toxic chloramines with HOCl. Amino acid-chloramines (RNHCl) were generated by reacting amino acids with HOCl, and showed maximum absorption near 250nm. Glycine, taurine, and β-alanine readily formed hydrophilic chloramines with high absorption at 250nm. The ESR spectrum of HOCl changed to that of RNHCl by reacting HOCl with each of these three amino acids. Taurine and β-alanine inhibited vascular endothelium lesions due to active oxygen species generated by neutrophils that had been stimulated by opsonized zymosan and phorbol myristate acetate.
This study examines the susceptibility to lipid peroxidation of rat heart and testis microsomes, in relation to dietary vitamin A and/or E status. Four groups of rats were fed different levels of the vitamins. After a period of 8 weeks, lipid peroxide levels estimated by thiobarbituric acid method, fatty acid composition and vitamins A and E were measured in serum or in microsomes. In heart, lipid peroxide levels were enhanced in dietary vitamin E deficiency; linoleic acid 18:2 (n-6), arachidonic acid 20:4 (n-6), and docosahexaenoic acid 22:6 (n-3) were significantly decreased. In testis, dietary vitamin A deficiency significantly increased lipid peroxide production and decreased docosapentaenoic acid 22:5 (n-6) and 20:4 (n-6). Supplementation of the diet with both vitamins A and E significantly decreased lipid peroxide production but did not change the fatty acid composition. Induced lipid peroxidation increased in the heart of vitamin E-deficient rats and in the testis of vitamin A-deficient ones. Both in heart and testis, we found a good correlation between spontaneous and induced lipid peroxides and also between lipid peroxides and polyunsaturated to saturated fatty acid ratio. Besides, lipid peroxide production was well correlated with polyunsaturated fatty acids/vitamin A in testis and with polyunsaturated fatty acids/vitamin E molar ratios in heart. Membrane susceptibility to lipid peroxidation varied greatly according to dietary status and organ. Vitamin E seemed to be a more effective antioxidant for heart, and vitamin A, for testis. Supplementation enhanced the beneficial role of each vitamin.
The insulin secretion expressed in terms of plasma concentration in response to an oral glucose load (1.8g per kg body weight) in biotin-deficient male Wistar rats was approximately one-sixth that of pair-fed controls. However, the insulin content of the pancreas in biotin-deficient rats was no lower than that of control rats. The reduction in insulin secretion in the biotin-deficient rats was reversed to a significant extent by the simultaneous administration of biotin (1mg per kg body weight) with the glucose solution. This suggests that biotin may play an important role in the secretion of insulin from the β-cells of the pancreas.
Ageing is associated with greater susceptibility to nutritional deficiencies and to progressive senescence of the immune system. Ascorbic acid has been reported to have a corrective influence on the alteration of immunological functions that occurs during ageing. We examined the effect of a daily oral dose of ascorbic acid (20mg/100g body weight for 15, 30, and 60 days) on immune responses in young and old rats. A significant increase was observed in the total leucocyte count in both young and old rats after 60 days of ascorbic acid supplementation. When rats were fed the normal diet, the values of phagocytosis, nitroblue tetrazolium reduction test, and soluble immune complex were lower in the older animals than in the younger. On supplementation with ascorbic acid, an increase in all these immunological functions was observed, the increment being highly significant in old rats after 60 days of ascorbic acid supplementation. Hence, our results suggest that dietary intake of ascorbic acid influences the cell-mediated immunity during the ageing process.
When 10-week-old male BALB/c mice received whole-body irradiation with a sublethal 4-Gy single dose of 60Co γ-ray, the occurrence of leucopenia caused by the irradiation was lessened to some extent by subcutaneous injection of 2-hydroxyestradiol (2-OHE2), one of catecholestrogens, given 3h before and 3h after the irradiation. Upon irradiation, the weight of the thymus was reduced, but the recovery of organ weight was markedly accelerated by subcutaneous injection of 2-OHE2. Light microscopic observation revealed that 2-OHE2 prevents the reduction by γ-ray irradiation of cortical and medullary volumes of the thymus. These results indicate that 2-OHE2 is a potent radioprotector.
The effects of simvastatin, a cholesterol biosynthesis inhibitor, on plasma lipoprotein concentrations and very-low-density lipoprotein (VLDL) secretion were investigated in the rat. The results showed that simvastatin did not significantly modify plasma lipid levels but did increase the cholesterol level of apolipoprotein E-rich high-density lipoproteins (+31%). The treatment significantly reduced total VLDL secretion (-26%), assessed by VLDL-triacylglycerol accumulation in plasma after lipolysis inhibition by Triton WR 1379. Since intestinal VLDL production, which was measured in rats fed orotic acid in order to block the hepatic secretion of lipoproteins, was not changed, we deduced that simvastatin reduced by 50% the hepatic VLDL secretion. Furthermore, whole-body cholesterol production, assessed by the sterol balance, appeared inhibited in the rat after long-term simvastatin treatment.