Induction of oxidative stress by arsenic in Clarias batrachus: Involvement of peroxisomes

Indian catfish, Clarias batrachus, were exposed to two nonlethal doses of arsenic for 10 days, which induced tissue lipid peroxidation, increased the ratio of oxidized to reduced glutathione and produced excess H2O2 within 1–2 days of exposure. Furthermore, arsenic treatment increased the activity of antioxidant enzymes such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase but decreased glutathione reductase (GR) activity within a day of exposure, indicating the generation of oxidative stress in fish at an early stage. Reversibility of these arsenic-induced responses by pretreatment with N-acetylcysteine indicates that the oxidative stress was due to excess H2O2 production, which was found to be partially contributed by altered H2O2 metabolism in the peroxisomes. It is therefore concluded that peroxisomal H2O2 metabolizing enzymes are potential targets of arsenic toxicity in C. batrachus.