The platelet survival time was shortened in stroke-prone spontaneously hypertensive rats (SHRSP) at 10 weeks of age on feeding the regular diet but it was normalized on administering the vitamin E-supplemented diet. Platelet survival time was normal in stroke-resistant spontaneously hypertensive rats (SHRSR) at 10 weeks of age on feeding the regular diet but it was shortened when supplying the vitamin E-free diet. The maximal uptake of 75Se-selenomethionine by platelets was in-creased in SHRSP at 10 weeks of age on feeding the regular diet. It was further increased in SHRSP on feeding the vitamin E-free diet. On the other hand, the increased maximal uptake of 75 Se-selenomethionine by platelets was normalized in SHRSP on feeding both the vitamin E-supplemented diet and the vitamin E-supplemented diet after administer-ing the vitamin E-free diet. Therefore, we concluded that the deficiency of vitamin E brought about the shortening of platelet survival time and enhanced platelet production.
Three-week-old weanling rats of Wistar and Sprague Dawley strains were fed on tryptophan-limited and nicotinic acid-free diets for 46 days and the following was observed. (1) Gain in body weight of the Sprague Dawley strain was significantly higher than that of the Wistar strain from the 10th day of feeding. (2) Tryptophan oxygenase [EC 126.96.36.199] activity in the Wistar strain was constant but was significantly increased in the Sprague Dawley strain during the latter period of this experiment. (3) The total amount of nicotinic acid, quinolinic acid, N1-methylnicotinamide and tryptophan in liver and kidney of the Sprague Dawley strain was significantly higher than that of the Wistar strain. (4) Total urinary nicotinic acid, quinolinic acid and N1-methylnicotinamide levels were not very different between the two strains, but it was observed that at the 38th day the levels in the Sprague Dawley strain were significantly higher than those in the Wistar strain. From the above result, it was presumed that the Sprague Dawley strain of rat was more resistant to deficiency of nicotinic acid than the Wistar strain fed on a low tryptophan and nicotinic acid-free diet. Aminocarboxymuconate-semi-aldehyde decarboxylase [EC 188.8.131.52] activities in livers of both strains dropped to half the original value at the end of the experiment. This change may indicate metabolic control of increase in flow from tryp-tophan to NAD.
Cell-free extracts of a facultative methylotroph and strict aerobe, Protaminobacter ruber, could catalyze formation of β-methylaspartate from glutamate. β-Methylaspartate formed was further converted to mesaconate. From these results, it was found that the cells of P. ruber contained a sequential reaction system of glutamate mutase and β-methylaspartase. The level of glutamate mutase activity was almost constant throughout the period of cultivation. When P. ruber was grown on several non-one-carbon compounds in addition to methanol as a sole carbon source, the activity of glutamate mutase was not markedly affected by the kinds of carbon sources.
The primary cause of the adverse effects of feeding of raw winged bean seeds in rats was investigated. In experiment 1, rats were fed on either a raw winged bean diet or a steamed winged bean diet for 10 days. Body weight gain of rats fed on 30% raw winged bean diet was significantly lower than that of rats fed on 30% steamed winged bean diet. The adverse effect of the feeding of 30% raw winged bean diet on growth was accompanied by disorders of the gastrointestinal tract including a significant reduction in intestinal sucrase activity, not being improved with feeding of the diet supplemented with methionine. In experiment 2, rats fasted for 2 days were refed on a 10% casein.diet, a 30% raw winged bean diet or a 30% steamed winged bean diet, in which most of the carbohyd-rate component was sucrose, for 4 days. Although body weight gain and food consumption in rats refed on these winged bean diets were lower than those in rats refed on 10% casein diet, the effects of feeding of the raw winged bean diet on body weight gain and food consumption were extremely deleterious as compared with those of feeding of the steamed winged bean diet. Significant reductions in hydrolase activities localized in the brush border membrane of the small intestine were found in rats refed on the raw winged bean diet prior to the occurrence of apparent disorders in the gastrointestinal tract. These findings suggest that the primary cause of the adverse effects of raw winged bean seed feeding is disorders in the small intestine caused by lectin or similar substances in raw winged bean seeds.
The application of carbon dioxide anesthesia to fish has been studied in order to find a method of transport of live fish. In the continuation of this study, the levels of arterial PaO2, PaCO2 and pH were examined in carp anesthetized with carbon dioxide. In the initial stage of the anesthesia, both PaO2 and PaCO2 increased. In the following stage, PaCO2 gradually decreased. An increase or decrease in PaO2 seems to depend on the levels of PaCO2 during anesthesia. On the other hand, ECG (electrocardiogram) profiles of anesthetized carp indicate that a gradual increase in `R-R interval is coupled with a gradual decline of the opercular rate.
The effects of sucrose and Acarbose (oc-glucosidase in-hibitor) feeding on the development of diabetes were studied in streptozotocin-treated rats. Rats were raised on four different dietary regimens, viz, a sucrose diet (46% of the total weight in the form of sucrose, 24% as starch), a starch diet (70% as starch), a standard diet (laboratory chow: Oriental Yeast Co.) or an Acarbose diet (a standard diet containing 75 mg Acarbose/ 100 g diet) for a week followed by an intraperitoneal injection of streptozotocin (70 mg/kg). Development of diabetes was determined by urinary and blood glucose levels (more than 250 mg/dl). The incidence of diabetes in the groups of rats fed on sucrose, starch, standard, and Acarbose diets was 100%, 80%, 70% and 47.6%, respectively. The development of diabetes was accelerated by sucrose feeding and depressed by Acarbose feeding. There was mild diabetes in rats fed on Acarbose diet. The sucrose feeding caused a marked increase of disaccharidase activities in the proximal part of the intestine and in the apical part of the villus-crypt gradient of epithelial cells. The Acarbose feeding caused a significant decrease of disaccharidase activities. The changes in protein content of the sucrase-isomaltase complex appeared to be in parallel with those of disaccharidase activities. These results suggest that intestinal disaccharidase activities are involved in the development of experimental diabetes induced by streptozotocin.
In rats fed for 2 weeks on a 10% casein diet suaolemented with 5% leucine, the hepatic NAD content was lowered when comparing with the control rats pair-fed on the 10% casein diet. The hepatic NAD glycohydrolase [EC 184.108.40.206] activity increased by 25% in the leucine-supplemented diet-fed rats and by 40% in the nicotinic acid-free diet-fed rats. The hepatic NAD glycohydrolase activity in the rats fed on the non-protein diet freely for 1 week was elevated by 60% compared to the rats fed on the 18% casein diet. The hepatic NAD content in the former animals was significantly lower than that in the latter. The 70% casein diet caused changes in neither hepatic NAD content nor NAD glycohydrolase activity. These results indicated an inverse relationship between hepatic NAD content and NAD glycohydrolase activity.