The effects of 96 h exposure to Cr6+ (added as potassium dichromate) on the status of antioxidant defenses and markers of oxidative damage were evaluated in three tissues of goldfish, Carassius auratus. Fish exposure to high dichromate concentrations, 10 and 50 mg/l, increased protein carbonyl levels in brain and liver, but not in kidney. Chromium exposure also increased concentrations of lipid peroxides in brain (at 5 mg/l) and liver (10 mg/l), but not in kidney. The concentrations of reduced glutathione (GSH) were higher in the liver of goldfish treated with 5-50 mg/l Cr6+ than in controls, but in kidney only the 5 mg/l-treated group showed increased GSH levels. Dichromate at 1 mg/l increased the concentration of oxidized glutathione (GSSG) in liver and kidney by 80% and 60%, respectively, whereas at 10 and 50 mg/l the levels of GSSG decreased by 50% in kidney. These results indicate that the dichromate concentrations used induced oxidation of lipids and proteins in goldfish tissues in a concentration- and tissue-specific manner. Also, the redox status of fish tissues was affected in a concentration- and tissue-specific manner. The activities of glutathione reductase increased in all three tissues in response to dichromate treatment, increasing by ∼2-fold in brain and liver in goldfish treated with 50 mg/l Cr6+. Dichromate treatment did not change the activities of SOD, catalase or GST in brain, but reduced the activities of SOD in liver and kidney, and catalase in liver. The results suggest that the glutathione system may be responsible for protecting against the deleterious effects of dichromate in fish and indicate the possible development of an adaptive response during the 96 h treatment with the toxicant.

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Aquatic Toxicology
Department of Biology

Lushchak, O.V. (Oleh V.), Kubrak, O.I. (Olha I.), Nykorak, M.Z. (Mykola Z.), Storey, K, & Lushchak, V.I. (Volodymyr I.). (2008). The effect of potassium dichromate on free radical processes in goldfish: Possible protective role of glutathione. Aquatic Toxicology, 87(2), 108–114. doi:10.1016/j.aquatox.2008.01.007