As bisphenol A (BPA) effortlessly crosses the blood-brain barrier, its serious impacts on the neuronal microenvironment towards precocious induction of oxidative stress and neuromorphological alteration can't be ignored. Incidentally, a symmetric study establishing the possible link of transformed neurobehavior with heightened monoamine oxidase (MAO) activity and neuromorphological alteration in zebrafish brain subsequent to BPA-exposure is limiting in the literature. The study was conducted to delineate the role of BPA towards the genesis of aggressive behaviour in zebrafish and its correlation with brain MAO activity. Mirror biting test and open field test were conducted to evaluate the aggressive and explorative behaviour respectively. Biochemical studies were performed to delineate the modulation of the antioxidant defence system. Cresyl violet staining and Hoechst staining in the periventricular grey zone of the zebrafish brain were conducted to evaluate neuronal pyknosis and chromatin condensation. Our study showed that BPA exposure is associated with the genesis of aggressive neurobehavioral response. Moreover, the brain MAO activity, oxidative stress and chromatin condensation were increased with increase in exposure duration. The results of the present study gave conclusive evidence that BPA act as a potent neurotoxicant in transforming the native neurobehavioral response of zebrafish through heightened oxidative stress, MAO activity and altered neuromorphology.
Keywords: Bisphenol A; Monoamine oxidase activity; Neurobehavioral response; Neurodegeneration; Oxidative stress; Zebrafish.
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