Russanov E M, Kassabova T A, Konstantinova S G, Balevska P S
Acta Physiol Pharmacol Bulg. 1986;12(1):51-6.
The activity of antioxidative enzymes SOD, catalase, glutathione peroxidase and the related glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-isocitrate dehydrogenase was examined in liver cytosol and large granule fraction (mitochondria) from control and copper-loaded rats. An increase of SOD activity (more than 100%) and a decrease of both catalase (by 60%) and glutathione peroxidase activity (by 30%) in large granule fraction were observed after copper loading. The cytosolic glutathione peroxidase activity was also markedly decreased: glutathione peroxidase I (EC 1.11.1.9)--by 35% and glutathione peroxidase II (EC 2.5.1.18)--by 75%. Cytosolic catalase activity and the glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-isocitrate dehydrogenase activities in cytosol and in mitochondria of copper-loaded rats were unchanged. It is concluded that under chronic copper loading the primary mechanisms of copper toxicity are accompanied by disturbances of the antioxidative enzyme function.
在对照大鼠和铜负荷大鼠的肝脏胞质溶胶和大颗粒部分(线粒体)中,检测了抗氧化酶超氧化物歧化酶(SOD)、过氧化氢酶、谷胱甘肽过氧化物酶以及相关的谷胱甘肽还原酶、葡萄糖-6-磷酸脱氢酶和NADPH-异柠檬酸脱氢酶的活性。铜负荷后,在大颗粒部分观察到SOD活性增加(超过100%),而过氧化氢酶活性降低(60%),谷胱甘肽过氧化物酶活性降低(30%)。胞质溶胶中的谷胱甘肽过氧化物酶活性也显著降低:谷胱甘肽过氧化物酶I(EC 1.11.1.9)降低35%,谷胱甘肽过氧化物酶II(EC 2.5.1.18)降低75%。铜负荷大鼠的胞质溶胶和线粒体中的胞质过氧化氢酶活性以及谷胱甘肽还原酶、葡萄糖-6-磷酸脱氢酶和NADPH-异柠檬酸脱氢酶活性均未改变。得出的结论是,在慢性铜负荷下,铜毒性的主要机制伴随着抗氧化酶功能的紊乱。