Induction of reactive oxygen species in brain of Etroplus maculatus after exposure to bisphenol A
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Abstract
The present study was aimed to investigate that bisphenol A, an environmental estrogen, exposed at 648 ?g/ 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 reduction
in 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 ?g/ 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.
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Acetyl cholinesterase, Bisphenol A, Brain, Etroplus maculatus, Oxidative stress, ROS
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