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Abstract Due to the continuous exposure to bisphenol-A (BPA), the current study was conducted to evaluate taurine’s neuroprotective action against BPA’s adverse effect on the brain. Rats were grouped into control, BPA-treated rats, and taurine + BPA-treated rats. At the end of the 35-day treatment period, the memory of the rats was evaluated using the novel object test and the Y-maze test. An open-field test was used to measure motor activity. The changes in monoamines, monoamine oxidase (MAO), acetylcholinesterase (AChE), Na + ,K + ,ATPase, oxidative stress, caspase-3, and histopathology were evaluated in the cortical and hippocampal tissues of all groups. Data analysis by ANOVA revealed that BPA treatment induced motor hyperactivity and short- and long-term memory impairment. In the cortex, BPA decreased serotonin (5-HT), norepinephrine (NE), MAO, Na + ,K + ,ATPase, and nitric oxide (NO) and increased dopamine (DA), AChE, lipid peroxidation (MDA), glutathione (GSH), and caspase-3. In the hippocampus, BPA increased 5-HT, DA, NE, MAO, AChE, MDA, NO, GSH, and caspase-3 and decreased Na + ,K + ,ATPase. These neurochemical changes were accompanied by significant histopathological alterations. Taurine treatment prevented memory impairment and motor hyperactivity induced by BPA. Taurine attenuated the neurochemical changes, oxidative stress, and caspase-3 level. Taurine improved the histopathological change induced by BPA. In conclusion, taurine significantly prevented BPA-induced cognitive deficits, motor coordination impairments, neurotransmitter imbalances, histopathological alterations, oxidative stress, and apoptosis.
Nazmy et al. (Fri,) studied this question.