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Biomedical subjects

G M Thie

Publications and source records attributed to G M Thie.

2 recordsLinked to original sources

Cytogenetic changes in fish exposed to water of the river Rhine.

The induction of chromosome aberrations in fishes, exposed to Rhinewater, was investigated. The mudminnow, Umbra pygmaea, was chosen for this study, because of its ideal karyotype of 22 large chromosomes. Gill cells were used for chromosome studies. Fish, kept in Rhinewater for 11 days had chromosome breaks in approximately 30% of the metaphases studied. Control fish, exposed to a very good quality of untreated groundwater had breaks in about 8% of the metaphases. Several Rhinewater extracts were tested for their mutagenic potential in the Salmonella-microsome test. The fraction of aromatic compounds was found to be positive. This may indicate that one or more of the compounds present in this fraction were also responsible for the cytogenetic changes found in the fish.

Animals

Effect of cholesterol feeding on tissue lipid perioxidation, glutathione peroxidase activity and liver microsomal functions in rats and guinea pigs.

The effect of cholesterol feeding on liver and aortic nonenzymatic lipid peroxidation and glutathione peroxidase activities, and on liver microsomal NADPH-dependent lipid peroxidation, codeine hydroxylation and cytochrome P-450 levels was examined in rats and guinea pigs. One percent cholesterol was added to a casein-sucrose-soybean oil basal diet for rats or a stock diet with 2% soybean oil for guinea pigs. The effect of vitamin E and cholestyramine was also examined in some experiments. Cholesterol feeding increased the rate of lipid peroxidation in liver and aortic homogenate both in rats and guinea pigs when fed non-vitamin E supplemented basal diets. Vitamin E supplementation prevented the increase in the aorta, but not as completely in the liver in rats, while the reverse was true in guinea pigs. The effect of cholestyramine was dependent on the level of vitamin E in the diet. Cholesterol feeding decreased glutathione peroxidase activities in rats and guinea pigs. In guinea pigs, cholesterol feeding also markedly decreased liver microsomal NADPH-dependent lipid peroxidation, codein hydroxylation and cytochrome P-450 levels especially when fed non-vitamin E supplemented basal diets. In rats, cholesterol feeding reduced liver microsomal NADPH-dependent lipid peroxidation and in some cases, increased microsomal codeine hydroxylation activities, but had no effect on microsomal cytochrome P-450 levels. Vitamin E supplementation increased liver and serum cholesterol levels in guinea pigs, but had no such effect in rats. Results of this study indicate that cholesterol feeding can result in various metabolic alterations in rats and guinea pigs. The implication of these alterations in atherogenesis requires further investigations.

Animals