Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, P.O. Box 533, H-6701 Szeged, Hungary.
Comp Biochem Physiol C Toxicol Pharmacol. 2013 Nov;158(4):225-30. doi: 10.1016/j.cbpc.2013.07.005. Epub 2013 Aug 3.
This study is related to the accumulation of Cd(2+), its effects on oxidative stress biomarkers and its role in macromolecule damage in liver and kidney of common carp. We present evidence of an increased ratio of reduced to oxidized glutathione (GSH/GSSG) in both organs after 10 mg/L Cd(2+) exposure, with different underlying biological mechanisms and consequences. In the liver, the expressions and/or activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase increased to cope with the Cd(2+)-generated toxic effects during the first 48 h of treatment. In contrast, none of these selected antioxidant markers was significantly altered in the kidney, whereas the expression of glutathione synthetase was upregulated. These results suggest that the major defense mechanism provoked by Cd(2+) exposure involves the regeneration of GSH in the liver, while its de novo synthesis predominates in the kidney. High levels of accumulation of Cd(2+) and peroxynitrite anion (ONOO(-)) were detected in the kidney; the major consequences of ONOO(-) toxicity were enhanced lipid peroxidation and GSH depletion. The accumulation of ONOO(-) in the kidney suggests intensive production of NO and the development of nitrosative stress. In the liver the level of hydrogen peroxide was elevated.
本研究涉及 Cd(2+)的积累、其对氧化应激生物标志物的影响以及在鲤鱼肝肾大分子损伤中的作用。我们提供的证据表明，在 10mg/L Cd(2+)暴露后，两种器官中还原型谷胱甘肽与氧化型谷胱甘肽的比例（GSH/GSSG）增加，其背后的生物学机制和后果不同。在肝脏中，超氧化物歧化酶、过氧化氢酶、谷胱甘肽还原酶和谷胱甘肽过氧化物酶的表达和/或活性在治疗的前 48 小时内增加，以应对 Cd(2+)产生的毒性作用。相比之下，在肾脏中，这些选定的抗氧化标记物均无明显变化，而谷胱甘肽合成酶的表达上调。这些结果表明，Cd(2+)暴露引起的主要防御机制涉及肝脏中 GSH 的再生，而在肾脏中则以其从头合成为主。在肾脏中检测到 Cd(2+)和过氧亚硝酸盐阴离子（ONOO(-)）的高水平积累；ONOO(-)毒性的主要后果是增强的脂质过氧化和 GSH 耗竭。肾脏中 ONOO(-)的积累表明 NO 的大量产生和硝化应激的发展。在肝脏中，过氧化氢的水平升高。
