Chromium-induced biochemical, genotoxic and histopathologic effects in liver and kidney of goldfish, carassius auratus.

Fish constitute an excellent model to understand the mechanistic aspects of metal toxicity vis-à-vis oxidative stress in aquatic ecosystems. Hexavalent chromium (Cr (VI)), due to its redox potential can induce oxidative stress (OS) in fish and impair their health. In the present investigation, we hypothesize that OS plays a key role in chromium induced toxicity in goldfish; leading to the production of reactive oxygen species (ROS) such as O(.)(2), H(2)O(2), OH(.), and subsequent modulation of the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), metallothioneins (MT), glutathione proxidase (GPx), genotoxicity and histopathology. To test this hypothesis, antioxidant enzymes, DNA damage and histopathology assays were performed in liver and kidney tissues of goldfish exposed to different concentrations of Cr (VI) (LC(12.5), LC(25) and LC(50)) following 96h static renewal bioassay. The results of this study clearly show that the fish experienced OS as characterized by significant modulation of enzyme activities, induction of DNA damage and microscopic morphological changes in the liver and kidney. In both tissues, CAT activity was decreased whereas SOD activity and hydroperoxide levels were increased. In addition, GPx activity also increased significantly in higher test concentrations, especially in the kidney. MT induction and DNA damage were observed in both tissues in a concentration dependent manner. Microscopic examination of organ morphology indicated degeneration of liver tissue and necrosis of central vein. Necrosis of kidney tubular epithelial cells and tubules was observed at higher Cr (VI) concentrations. Taking together the findings of this study are helpful in organ-specific risk assessment of Cr (VI)-induced oxidative stress, genotoxicity and histopathology in fish.