The present study was designed to assess the effect of chlordecone on the stimulation of oxidative stress in gill, liver and brain tissues of the cichlid fish, Pseudetroplus maculatus. Fishes were exposed to chlordecone at two sublethal concentrations, 3.5 and 7 μg/L, for 24, 72 and 96 h, maintaining ten animals in each group. Chlordecone treatment did not alter the body weight of the animal. However, significant increase in the secretion of mucous and decrease in the weights of gill, brain and hepatosomatic index were observed at 7 μg/L of chlordecone treatment only after 96 h. Gill tissue showed significant increase in the activities of superoxide dismutase, catalase and glutathione reductase along with elevated levels of hydrogen peroxide and lipid peroxidation in concentration and timedependent manner. This could be the defensive mechanism of gill tissue to escape the toxic effects of chlordecone. In the liver tissue, superoxide dismutase activity was increased by 39% at 3.5 μg/L and by 73% at 7 μg/L of chlordecone treatment. Activities of catalase and glutathione reductase were decreased 3 to 9 times at 3.5 and 7 μg/L concentrations, respectively, with concomitant increase in hydrogen peroxide generation (17 to 28 times) and lipid peroxidation (3 to 7 times) at the end of 96 h, which reveals the failure of hepatic antioxidant system to prevent free radical generation owing to chlordecone exposure. Activities of all antioxidant enzymes in the brain were inhibited by 29 to 80% along with the induction of hydrogen peroxide (13 to 20 times) and lipid peroxidation (6 to 11 times), thereby indicating imbalance in the antioxidant status. Activities of gill and liver marker enzyme - alkaline phosphatase - and acetylcholinesterase in brain were decreased. Therefore, imbalance in the antioxidant defence system as a result of chlordecone toxicity could lead to susceptible oxidative stress in various tissues of the fish.

Abstract. The present study was designed to evaluate the effects of nonylphenol in the pro-oxidant/ antioxidant system in ovary of the cichlid fish Etroplus maculatus. Fishes were exposed at two sublethal concentrations (one-fifth and one-tenth of LC 50 ) of nonylphenol for 24, 72 and 96 h maintaining control groups. The oxidative stress indices as the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase along with the levels of hydrogen peroxide generation and lipid peroxidation were monitored in concentration-and time-dependent manner. Activity of superoxide dismutase significantly (P<0.05) increased at both concentrations in timedependent manner. Meanwhile the activities of catalase and glutathione reductase significantly (P<0.05) decreased after 72 and 96 h of nonylphenol treatment. The levels of hydrogen peroxide generation and lipid peroxidation increased in all treatment groups when compared to controls. The present results demonstrated that the induction of oxidative stress in ovary of fish by the generation of lipid peroxidation could be due to the exposure of environmental contaminant, nonylphenol. Therefore, the observed oxidative stress in ovary can be indicated as a mechanism of toxicity in the fish exposed to nonylphenol.

The present study was designed to evaluate the effects of nonylphenol in the pro-oxidant/ antioxidant system in ovary of the cichlid fish Etroplus maculatus. Fishes were exposed at two sublethal concentrations (one-fifth and one-tenth of LC50) of nonylphenol for 24, 72 and 96 h maintaining control groups. The oxidative stress indices as the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase along with the levels of hydrogen peroxide generation and lipid peroxidation were monitored in concentration-and time-dependent manner. Activity of superoxide dismutase significantly (P<0.05) increased at both concentrations in time-dependent manner. Meanwhile the activities of catalase and glutathione reductase significantly (P<0.05) decreased after 72 and 96 h of nonylphenol treatment. The levels of hydrogen peroxide generation and lipid peroxidation increased in all treatment groups when compared to controls. The present results demonstrated that the induction of oxidative stress in ovary of fish by the generation of lipid peroxidation could be due to the exposure of environmental contaminant, nonylphenol. Therefore, the observed oxidative stress in ovary can be indicated as a mechanism of toxicity in the fish exposed to nonylphenol.

The present study was aimed to investigate that bisphenol A, an environmental estrogen, exposed at 648 μg/ L concentration for 96 h could induce reactive oxygen species in brain of cichlid fish, Etroplus maculatus. Evaluation of antioxidant enzymes as superoxide dismutase, catalase and glutathione reductase showed a reductionin the activities at 5% level of significance with concomitant increase in the level of hydrogen peroxide generation (from 1.546 ± 0.426 (control), 1.506 ± 0.217 (DMSO) to 1.888 ± 0.368 (24 h), 5.332 ± 0.589 (72 h), 2.392 ± 0.341 (96 h)) and lipid peroxidation (from 2.805 ± 0.33 (control), 2.401 ± 0.309 (DMSO) to 3.596 ±0.373 (24 h), 5.65 ± 0.306 (72 h), 3.834 ± 0.236 (96 h)). The brain marker enzyme, acetylcholinesterase decreased at 24, 72 and 96 h in time-dependent manner than that of control groups. The present findings summarize that the increased production of oxygen free radicals due to the exposure of an environmental estrogen, bisphenol A at sub lethal concentration (648 μg/ L) for 96 h inhibited the activities of antioxidant enzymes thereby induced oxidative stress in brain of fish. The decreased activity of brain marker enzyme, acetylcholinesterase reflect the neurotoxicity of bisphenol A in brain of fish, Etroplus maculatus and this could be one of the possible mechanisms of bisphenol A-induced neurodevelopmental disorders in fish.