Biomedical subjects
Publications and source records attributed to Y Yamane.
Uptake of Li+ induced by the addition of proline to a cell suspension of Escherichia coli was detected using an Li+-selective electrode. This Li+ uptake was inhibited by L-azetidine 2-carboxylic acid, a competitive inhibitor of the proline transport system. Thus, direct evidence for Li+-proline cotransport via the proline transport system was obtained. Kinetic parameters of the Li+ uptake were determined.
The effect of zinc on mercuric chloride-induced lipid peroxidation in the rat kidney was investigated. The rats received zinc acetate (2.0 mmol/kg, po) for 2 days before being given mercuric chloride (15 mumol/kg, sc) and were killed 6, 12, and 24 hr after the last injection. Lipid peroxidation occurred in the rat kidney 12 hr after mercury administration, and this mercury-induced lipid peroxidation was significantly reduced by zinc pretreatment. A decrease in vitamin C and E contents in the kidney was observed 12 hr after the administration of mercury, and this decrease was prevented by zinc pretreatment. In the kidney of rats pretreated with zinc, the activities of the protective enzymes, glutathione peroxidase and glucose-6-phosphate dehydrogenase, were increased after mercury injection. Non-protein sulfhydryl content (mostly glutathione) also rose markedly. The results indicate that zinc not only induces metallothionein, but also increases protective enzyme activities and glutathione content, which would tend to inhibit lipid peroxidation and suppress mercury toxicity.
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The effect of cupric acetate on dimethylnitrosamine (DMN)-induced hepatocarcinogenesis in rats was investigated. The surviving rats in the group given DMN (25 ppm) in the drinking water alone were killed at 26 weeks and it was found that 12 of 16 rats had developed liver tumors. In the group given DMN and cupric acetate (sc injections of 2 mg of Cu/kg of body weight once a week for 26 weeks), 7 of 22 rats developed liver tumors. The incidence of liver tumors in rats given DMN and cupric acetate was thus only about 40% of that in rats given DMN alone. No tumor was observed in the group given saline or cupric acetate alone. The thymidine incorporation into the liver DNA of rats was measured at 2 and 4 weeks after the start of the carcinogenicity experiment. The thymidine incorporation into the liver DNA of rats given DMN was significantly suppressed by the administration of cupric acetate. The methylation of liver DNA in rats given a single dose of DMN was also significantly suppressed by sc injection of cupric acetate; the formation of both O6-methylguanine and 7-methylguanine was reduced. This result suggests that sc injection of cupric acetate may have a suppressive effect on the initiation of carcinogenesis in the liver.
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Observations were made of the biological effects on infection with plerocercoids of Spirometra erinacei on normal female Snell mice, male chinese hamsters, golden hamsters, normal and hypox rats. Plerocercoid infection caused the strongest growth-promoting effect on normal Snell mice. In mice, this effect appears to be independent of strain. Chinese hamsters infected with these larvae showed similar growth. The infected normal rats and golden hamsters, however, showed a weight increase in the skeletal muscle only, while the hypox rats exhibited no effect at all. The elevation in the concentration of serum triglyceride was observed in all the animals investigated except for rats. Golden hamsters, in particular, exhibited a marked increase in the concentration of serum free fatty acids and total cholesterol. There was close correlation between the concentrations of serum triglyceride and free fatty acids, and the regression coefficient of the resulting linear regression equation for the experimentals was higher than that for the controls. This suggests that serum triglyceride results from an increased concentration of serum free fatty acids derived from stimulated lipolysis. The total cholesterol concentration in the serum decreased in chinese hamsters infected with larvae. The serum glucose concentration increased in normal Snell mice but decreased in chinese and golden hamsters. No difference in glycerol and free fatty acid concentration was observed in infected animals except for golden hamsters.
The ratio of CMV virus released into the supernatant per infected human fibroblast was studied for three laboratory strains and seven fresh isolates. The former all gave ratios over one whereas the latter gave ratios less than one. This phenomenon may serve as a marker of high passage attenuated virus, as about 25 passages were required in case of one strain to change this property.
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Dose-related suppression of the 3H-thymidine incorporation into liver DNA of rats after a single injection of dimethylnitrosamine by copper pretreatment was observed. The 3H-thymidine incorporation was not decreased by cadmium pretreatment. On the other hand, the 3H-thymidine incorporation into liver DNA of partially hepatectomized rats was decreased by both copper and cadmium pretreatments. Thymidine kinase activity in the liver of rats treated with dimethylnitrosamine was also decreased by copper pretreatment, but the enzyme activity was not decreased by cadmium pretreatment. Copper accumulation in the liver of copper-administered rats was predominantly in the nuclear fraction, followed by the soluble fraction. Cadmium accumulation in the liver of cadmium-administered rats was predominantly in the soluble fraction, followed by the nuclear fraction. Copper accumulation in the nuclear fraction may suppress the induction of thymidine kinase in the liver of rats by dimethylnitrosamine.