X-irradiation effects on lipid peroxidation and superoxide dismutase and catalase activities in copper deficient and copper loaded rat liver.

The whole body X-irradiation was found to intensify the lipoperoxidative processes in rat liver mitochondria and microsomes, which resulted in a two-fold increase of hydroperoxides in the membrane lipids. The moderate copper-loading of the liver cell had a protective effect against X-ray induced lipid peroxidation. The X-ray influence on the superoxide dismutase (SOD) and catalase activity in normocupric state, copper deficiency and copper loading was also studied. The latter two states were used as models of altered enzyme activity. Copper deficiency decreased the specific SOD activity in both mitochondrial fraction and cytosol, while the increased copper cell content activated this enzyme in mitochondria and did not change it in cytosol. Irradiation inhibited SOD in all preparations studied, with the exception of cytosol upon copper deficiency. Whatever the cell level of copper, X-ray exposure resulted in a decrease of catalase activity in cytosol, while in the mitochondrial fraction, including peroxisomes, the irradiation effects were different. It was found that both SOD and catalase after whole-body irradiation exhibited a higher specific activity in mitochondrial fraction upon copper loading compared with normocupric state, which correlates with the delayed lipid peroxidation processes.