Author
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Johnson, William |
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Submitted to: Experimental Biology
Publication Type: Abstract Only Publication Acceptance Date: 4/17/1999 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Food restriction may ameliorate oxidative damage caused by copper (Cu) deficiency. In the present study, four groups of male, weanling rats were fed Cu-deficient (CuD) and Cu-adequate (CuA) diets ad libitum and Cu- deficient (CuD80) and Cu-adequate (CuA80) restricted to 80% of the ad libitum consumption. Cytochrome c oxidase (CCO) activity decreased and manganese superoxide dismutase (MnSOD) activity increased in liver and heart mitochondria of rats fed CuD and CuD80. Food restriction decreased MnSOD activity in liver mitochondria independently of Cu status, but in heart mitochondria, MnSOD activity was lower (P<0.05) in rats fed CuD80 (6.3 Units/mg) than in rats fed CuD (8.2 Units/mg). Food restriction did not affect CCO activity. Heart mitochondrial glutathione peroxidase (GPX) activity was not affected by food restriction but was elevated in rats fed CuD and CuD80. Increased MnSOD and GPX activities indicate that mitochondria are responding to oxidative stress and the decreased MnSOD activity suggests that food restriction lowers that stress. Oxidative stress during copper deficiency also was indicated by alterations in the electrophoretic patterns of mitochondrial proteins containing reactive carbonyl groups. However, the altered patterns were not influenced by food restriction. Although Cu deficiency may increase oxidative stress in mitochondria by lowering CCO activity, neither increased MnSOD and GPX activities nor food restriction are sufficient to prevent oxidative damage to mitochondrial proteins. |
