Lushchak Oleh V, Kubrak Olha I, Torous Ihor M, Nazarchuk Tetyana Yu, Storey Kenneth B, Lushchak Volodymyr I
Department of Biochemistry, Precarpathian National University named after Vassyl Stefanyk, 57 Shevchenko Str., Ivano-Frankivsk, 76025, Ukraine.
Chemosphere. 2009 Mar;75(1):56-62. doi: 10.1016/j.chemosphere.2008.11.052. Epub 2009 Jan 21.
Although information on the effects of Cr(6+) in biological systems is abundant, Cr(3+) has received less attention. Toxic effects of chromium compounds are partially associated with activation of redox processes. Recently we found that Cr(6+) induced oxidative stress in goldfish tissues and the glutathione system was shown to play a protective role. The present study aimed to investigate free radical processes in brain of goldfish exposed to CrCl(3). Trivalent chromium at a concentration of 50 mg L(-1) was lethal and therefore we chose to examine sublethal dosages of 1.0-10.0 mg L(-1) in aquarium water. The levels of lipid peroxides and protein carbonyls (measures of oxidative damage to lipids and proteins) in brain increased after 96 h exposure of goldfish to Cr(3+). However, exposure to 1.0-10.0 mg L(-1) Cr(3+) decreased total glutathione concentration in brain by approximately 50-60%. Oxidized glutathione levels also fell by approximately 40-60% except at the 10.0 mg L(-1) dosage where they decreased by 85%. Therefore, 10.0 mg L(-1) Cr(3+) significantly reduced the ratio [GSSG]/[totalGSH] to 35% of the control value. Chromium treatment did not affect the activity of superoxide dismutase, but reduced the activities of catalase by 55-62% and glutathione-S-transferase by 14-21%. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were unchanged under any experimental conditions used. Therefore, it can be concluded that although Cr(3+) exposure induced oxidative stress in goldfish brain, it failed to enhance the efficiency of the antioxidant system in the organ.
尽管关于六价铬在生物系统中的作用的信息很多,但三价铬受到的关注较少。铬化合物的毒性作用部分与氧化还原过程的激活有关。最近我们发现六价铬会在金鱼组织中诱导氧化应激,并且谷胱甘肽系统显示出起到保护作用。本研究旨在调查暴露于三氯化铬的金鱼大脑中的自由基过程。浓度为50mg/L的三价铬是致命的,因此我们选择在水族箱水中检测1.0 - 10.0mg/L的亚致死剂量。金鱼暴露于三价铬96小时后,大脑中脂质过氧化物和蛋白质羰基(脂质和蛋白质氧化损伤的指标)水平升高。然而,暴露于1.0 - 10.0mg/L的三价铬会使大脑中总谷胱甘肽浓度降低约50 - 60%。氧化型谷胱甘肽水平也下降了约40 - 60%,但在10.0mg/L剂量下下降了85%。因此,10.0mg/L的三价铬显著将[氧化型谷胱甘肽]/[总谷胱甘肽]的比例降低至对照值的35%。铬处理不影响超氧化物歧化酶的活性,但使过氧化氢酶的活性降低了55 - 62%,谷胱甘肽 - S - 转移酶的活性降低了14 - 21%。在任何实验条件下,葡萄糖 - 6 - 磷酸脱氢酶和谷胱甘肽还原酶的活性均未改变。因此,可以得出结论,尽管暴露于三价铬会在金鱼大脑中诱导氧化应激,但它未能提高该器官中抗氧化系统的效率。