The effects of vitamin B2-acid on both cytochrome c red-uctase and diaphorase activities of ferredoxin-NADP+ reductase [EC 184.108.40.206] were investigated with enzyme kinetics. Vitamin B2-acid was shown to serve as an electron carrier for the two activities, as well as riboflavin or flavin mononucleotide (FMN). The two activities, however, were irreversibly affected by the preincubation of the enzyme with vitamin B2-acid under certain conditions, while riboflavin or FMN did not show such effects.
A study was conducted to examine the inhibitory effect of acyclic retinoid (polyprenoic acid) on the secretion of α-fetoprotein (AFP) in rats with chronic liver damage induced by CCl4. Oral ad-ministration of the compound brought about a significant reduction of serum AFP levels at the time when liver cirrhosis was formed. Acyclic retinoid also decreased the activities of serum aminotransferases and ornithine carbamyl transferase, while it increased serum albumin levels, demonstrating the reduction of hepatic parenchymal damage. Significant negative correlation was observed between serum AFP and albumin levels. This cytoprotective effect of the retinoid on the parenchymal cell may well be related to the inhibition of the synthesis and/or secretion of AFP. No significant side effect was observed, despite a long-term ad-ministration of the compound. The present finding will provide a po-tential scope for the future use of acyclic retinoid for the treatment of chronic liver damage.
The biosynthesis of biotin-vitamers from various carbon sources by the members of the Enterobacteriaceae as one of the groups of intestinal bacteria was investigated. The biotin-vitamers synthesized in each case included one or more of dethiobiotin (main product), 7-keto-8-aminopelargonic acid, and biotin. True biotin was shown to be synthesized under aerobic conditions but not under anaerobic conditions by each of several strains belonging to one of the genera, Erwinia, Escherichia, Proteus, and Serratia, and using culture media containing one of galactose, peptone, Polypepton, or casamino acid. In addition, a biotin precursor, pimelic acid, was also synthesized by several bacteria utilizing carbon sources such as maltose, mannose, galactose, peptone, or casamino acid.
We conducted experiments to elucidate the mechanism by which α-tocopheryl (α-toc) concentration in the liver remarkably in-creases in rats treated with polychlorinated biphenyls (PCB) when excess amounts of DL-α-tocopheryl-acetate (α-toc-ac) were given. First, diets containing 5 and 50mg of α-toc-ac per 100g were respectively added with 0.05% of PCB and given to rats for 10 days, and α-toc distributions in tissues were determined. Next, the disappearance of α-toc from a ligated intestine of vitamin E (E)-deficient rats was then studied. There were no significant differences between the control and the PCB groups in α-toc concentrations in the liver and other tissues except a few tissues when a lower level of a toc-ac (5mg) was given. Conversely, when a higher level of α-toc-ac (50mg) was given, α-toc concentration in the liver of the PCB group significantly increased compared to that of the control group. This agrees with the result previously reported, showing a remarkable repro-ducibility. In addition, α-toc concentrations in tissues other than the liver were also significantly higher in the PCB group than in the control group. Transmigration of α-toc to the liver from other tissues was therefore excluded. The α-toc absorption test using the ligated intestine of Edeficient rats revealed that α-toc disappears from the intestine at a higher rate in the presence of PCB compared to the untreated control group. This may indicate that α-toc absorption by passive diffusion is accelerated in the coexistence of PCB.
The effects of a threonine-imbalanced diet (8% casein supplemented with 0.3% methionine, TI) on the ketone body production and the secretion rate of lipids were examined in the isolated perfused rat liver. Feeding a TI diet compared to an 8% casein (C) diet resulted in an enlargement of liver, presumably due to 2-4-fold accumulation of triglyceride. Serum triglyceride likewise increased significantly in rats fed a TI diet. No significant difference was found in the other lipid components both in serum and liver. When the livers from rats fed C or TI diets were isolated and perfused in the presence of an exogenous oleate substrate, the TI diet decreased the ketone body production and conversely increased the secretion rate of triglyceride, suggesting an inverse relationship between rates of ketogenesis and triglyceride secretion. The proportion of oleate in the perfusate triglyceride obtained at the end of perfusion was comparable between the C and TI groups, whereas in the post-perfused liver it was higher in the former than in the latter, suggesting a stimulatory effect of the TI diet on the secretion of the oleate in the form of triglyceride. These results indicate that altered hepatic metabolism of long-chain free fatty acids between the pathways of oxidation and esterification is one of the causative factors for triglyceride accumulation in the liver produced by threonine imbalance.
The effect of diets containing the cells of a phototrophic bacteria (PTB), Rhodopseudomonas capsulata, on lipid metabolism was examined in the serum and liver of rats. Three groups of rats, 5 animals per group, were fed either a diet containing 0.2 or 2.0% PTB cells or a casein-based control diet. Each diet contained 1 % cholesterol (CHOL). While serum glucose levels were not significantly different between the control and the PTB groups, total CHOL and triacylglycerol (TG) in the serum were significantly lower in the PTB groups than in the control group (p<0.01). The ratio of serum HDL-CHOL to total serum CHOL was significantly higher in the PTB groups than in the control group (p< 0.01). The 2.0% PTB group had lower hepatic TG (p<0.05) but higher hepatic CHOL (p<0.05) than did the control group. These results indicate that PTB cells contain a factor or factors which affect hepatic metabolism or secretion of CHOL.
An experiment was conducted with growing rats to inves-tigate the effects of feeding excessive specific L-amino acids for 8 days on serum and tissue cholesterol, α-tocopherol, ascorbic acid, and copper, and on liver microsomal cytochrome P-450. To a 10% casein diet were added 4% L-methionine, 5% L-cystine, 5% L-histidine, 5% L-threonine, 5% L-tryptophan, 5% L-phenylalanine, 5% L-tyrosine, 6% L-valine, 7% L-isoleucine, 7% L-lysine, or 8% L-leucine. Excessive cystine and histi-dine increased serum cholesterol and α- tocopherol. Excessive cystine and methionine increased liver and kidney α-tocopherol and ascorbic acid. Excessive tyrosine and phenylalanine caused a marked increase in serum copper and ceruloplasmin activity, whereas excessive cystine, methionine, and histidine caused a decrease in the ceruloplasmin activity. Excessive histidine increased liver cytochrome P-450, whereas excessive tyrosine markedly decreased liver cytochrome P-450.
The purpose of this study was to determine effects of oral stimulation of sucrose on the diurnal output of pancreatic secretion in conscious dogs. Male beagle dogs weighing 9-11kg were prepared with gastric and duodenal fistulae. Once a day at 14:00 the animals were trained to eat a sufficient amount of a commercial stock diet to maintain their body weight. Gustatory receptors were stimulated at 9:00, 13:00, 15:00, and 18:00 for 5min with 100ml of 0.5% agar solutions containing 0.3M sucrose. Pancreatic juice was collected every 5 min before and after stimulation, and volume flow and protein output were measured. As a result, we demonstrated daily fluctuations timed by feeding not only in the pancreatic basal secretions but also in pancreatic responses to the gustatory stimulation. These results suggest the significant role of taste stimuli in the nutrition of, at least digestion in, animals.
The antioxidant activities of ubiquinol and ubiquinone were measured in the free radical-mediated oxidations of methyl linoleate in solution and phosphatidylcholine liposomes in aqueous dispersion. Ubiquinol-10 suppressed the oxidation of methyl linoleate in hexane, although its reactivity toward peroxyl radical was about 10 times less than that of a tocopherol. Ubgquinone-10, on the contrary, did not show any antioxidant activity. On the other hand, Ubiquinol-10 inhibited the oxidation of phosphatidylcholine liposomal membranes as efficiently as α-tocopherol. When both ubiquinol-10 and α-tocopherol were present, ubiquinol-10 decreased first and α-tocopherol decreased after all ubiq-uinol-10 was consumed in both solution and liposomes. These results and electron spin resonance (ESR) study suggest that ubiquinol-10 regenerates α-tocopherol by reducing α-tocopheroxyl radical.