An alkaline saponification method containing pyrogallol is usually applied for the determination of tocopherols. Although there are some metabolites of α-tocopherol in tissues, it is not yet clear whether they are true metabolites or degradation products from the alkaline saponi-fication. Since it was shown that α-tocopheryl spirodimer, a metabolite of α-tocopherol, was degraded mainly to a substance positive to Emmerie-Engel reagent, the identification of this substance was carried out. As the model compound of α-tocopherol (α-T), mainly 2, 2, 5, 7, 8-penta-methyl-6-hydroxy-chromane (M) was used. The results obtained showed that spirodimers of α-T and M were reduced to the corresponding di-hydroxydimers with pyrogallol during the saponification. Therefore, it was suggested that the alkaline saponification method could not be applied to detect the metabolites from α-T and related compounds.
This study was carried out on a correlation between simultaneous mater-nal and fetal serum vitamin E levels in 112 mothers and cord blood of their infants at delivery. Among the mothers, 55 were supplemented with vitamin E acetate prior to the delivery. The mean serum vitamin E level in the mother's blood and the cord blood was significantly higher in the vitamin E-supplemented group than in the control group, although the difference in the mean level between the two groups was very small in the cord blood, as compared with the maternal blood. A moderate correlation was noted between the cord blood and the mother's blood (γ=0.604, 0.522 and 0.567 for the total number of cases, the vitamin E-supplemented group and the control group, respectively). Changes in the incidence of the cases with positive erythrocyte hemolysis test in hydrogen peroxide, which were observed in the vitamin-E supplemented group, as compared with the control group, were statistically not signifi-cant.
The determination of adrenal glucose-6-phosphate dehydrogenase (G-6-PD) activity and electron microscopic observations of the adrenals of rats treated simultaneously with dexamethasone phosphate and flavin adenine dinucleotide (FAD) were carried out in order to clarify one of the preventive mechanisms of FAD on steroid-induced adrenal atrophy. The result showed that decrease of adrenal G-6-PD activity was pre-vented by simultaneous administration of FAD and dexamethasone phosphate. Electron microscopy of the fascicular zone of the adrenals of rats suggests that their function is depressed by dexamethasone phosphate alone but not by dexamethasone phosphate plus FAD. It is thought that the preventive effects of FAD on the steroid-induced adrenal atrophy are closely related to the preservation of adrenal G-6-PD activity.
Distribution of quinolinate phosphoribosyltransferase (an intermediary enzyme of NAD de novo biosynthesis) in animals, plants and microorgan-isms were investigated by radioassay using quinolinic acid-2, 3, 7, 8-14C as substrate. The enzyme activity was found to be widely distributed in nature. High activities were observed in rat liver, persimmon leaf, cucumber, Shiitake mushroom, Enokitake mushroom, baker's yeast, Pseudomonas riboflavina and Neurospora crassa. In mammals, signi-ficantly high activity was found in liver and kidney, but some activities were detected in brain and spleen. In some of fish livers, plants and microorganisms, the enzyme activity was not detected. The results suggest the possibility that another de novo biosynthetic pathway of NAD, which does not pass through quinolinic acid as an intermediate, may exist in those organisms.
The vitamin B12-binding capacity in bovine, pig and rat eye tissue extracts have been investigated in vitro. The B12-binding capacity in decreasing order was: cornea, retina, optic nerve and lens in bovine eye tissue extracts; cornea, retina, optic nerve and lens in pig eyes; and cornea, optic nerve and lens in rat. There are differences in B12-binding capacity in individual eye tissue extracts. However, no interspecies differences in the B12-binding capacity were found among bovine, pig, and rat eye tissue extracts, especially in the cornea, lens, retina and optic nerve in vitro.
1) Thiamine monophosphate kinase absolutely required a certain mono-valent cation, especially K+, for activity. 2) Enzyme activity was inhibited by ATP at high concentrations, and the inhibition was found to be due to a certain degree to the chelating action of Mg++. 3) Enzyme activity was scarcely affected by the intracellular concentra-tion of thiamine pyrophosphate.
The effects of lysine supplementation on the growth depression causes by the excessive addition of some individual amino acids to a wheat gluten diet in which lysine is the first-limiting amino acid were studied. Male weanling rats were fed 11.6% wheat gluten (equivalent to the N content of 10% casein) diets containing 5.0% of single amino acids, L-arginine-HCI, L-tryptophan, L-phenylalanine, L-methionine and L-tyrosine, with or without 0.6% of L-lysine ⋅HCl for 3 weeks. The growth retardation produced by the excess arginine was reversed by the sup-plement of lysine, but the adverse effects caused by the excessive addition of the other amino acids were not alleviated. The moderate elevations of arginine and lysine levels in blood plasma produced by excess arginine diet did not altered by the supplemental lysine. In contrast, the plasma levels of phenylalanine, tyrosine, tryptophan and methionine elevated by the excessive feeding of corresponding amino acid were decreased fairly by the supplement of lysine. The activities of liver arginase did not changed appreciably by the addition of excess arginine and the supplemental lysine. It is suggested that the decrease in growth when excess arginine is added to lysine-deficient diet causes the reduction of lysine utilization and increases need for lysine.
Rats were fed diets containing different levels of protein with or without pyridoxine. The growth of rats receiving the high-protein diet without pyridoxine was severely retarded. The total contents of pyridoxal in tissues and pyridoxic acid in urine were measured and the following results were obtained. In the liver, the pyridoxal content of rats receiving the high-protein diet was higher than that of rats receiving the low-protein diet, but in other tissues tested, the reverse situation was found. The pyridoxine-deficient rat fed on the high-protein diet showed severe decreases of pyridoxal levels in all the tissues examined. The pyridoxine-deficient rats excreted more pyridoxic acid in the urine than the intake, regardless of the protein levels of the diet. Some relationship between protein intake and excretion of pyridoxic acid is discussed.