Deciphering the putative role of stress paradigm on neurobehavioral response of zebrafish Implication of taurine towards therapeutic intervention
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Abstract
In our daily life we go through various kinds of stress that affects our health in later stages of life. However, literature is limiting with regard to the effect of various kinds of stress in inducing neurotoxicity and their amelioration through natural compound intervention. The current study was designed to find out the effect of waterborne exposure to the anthropogenic xenotoxicant bisphenol A (BPA) and chronic unpredictable stress (CUS) in inducing neurodegenerative phenotypes in zebrafish. Additionally, the role of chronic unpredictable stress in inducing neurobehavioral and neuromorphological alterations was studied. Our observation suggest that temporal exposure to BPA-induced neurobehavioral and neuromorphological alterations is associated with the increased monoamine oxidase (MAO) levels in the zebrafish brain. Furthermore, BPA-induced neurotoxicity leads to a decrease in brain derived neutrophic factor (BDNF) protein expression. Moreover, tyrosine hydroxylase (TH) protein expression was also decreased in BPA-exposed groups. The increased JNK protein expression was associated with alterations in mRNA expression of the apoptosis related genes. As a prophylactic measure, taurine reversed the neurobehavioral, biochemical and neuromorphological changes in the zebrafish brain. Also, the BPA-induced altered protein and mRNA expressions were ameliorated by taurine supplementation. Similarly, CUS-induced neurobehavioral and neuromorphological alterations and increased MAO levels was rescued by taurine co-supplementation.
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