Effect of chronic copper loading on the functions of rat liver mitochondria.
Male albino rats were kept on copper-enriched diet for 2, 4, 6 and 8 weeks. Experiments were made to study the electron transported, oxidative phosphorylation and the activity of some respiratory enzymes (rotenone-insensitive NAD. H-cytochrome c-reductase, NAD. H-DCPIP-reductase, succinate-cytochrome c(DCPIP)-reductase and succinate dehydrogenase) depending on the duration of copper sulphate treatment and hepatic copper level. Copper content is found to rise as early as the 2nd week, after which it remains relatively constant. Oxygen consumption in State 3 decreases strongly during the 2nd week and remains low throughout the period studied. Oxygen consumption in State 4 also decreases in the 2nd week, after which it rises and reaches the values of the control animals. The enzyme activities studied are also strongly inhibited (32-57%) after a 14-day treatment, later they are recovered gradually, reaching 50-79% of the control values. The probable compensatory mechanism of copper metabolism in the liver and the participation of thiol groups in it are discussed.
D000818:Animals; D003300:Copper / Q000494:pharmacology*; D004032:Diet; D004789:Enzyme Activation / Q000187:drug effects; D008099:Liver / Q000187:drug effects; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000201:enzymology; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D013347:Subcellular Fractions / Q000187:drug effects; D013997:Time Factors
D003300:Copper