Objective: Bisphenol A (BPA) has been found to exert neurotoxic effects through its neuroendocrine disruption and generation of reactive oxygen species (ROS). It can also cross the blood-brain barrier altering spatial learning and memory leading to cognitive impairment (Birla et al., 2019). We set out to explore compounds that could offer neuro-protection following BPA-induced neurotoxicity.

Background: Bisphenol A (BPA) is a common industrial chemical used in the manufacture of plastics and epoxy resins. It is an endocrine disrupting chemical implicated in several adverse health effects such as cancer, diabetes, etc. Gallic acid (GA) is one of the most abundant phenolic acids in fruits and plants reported to have antioxidant and neuro-protective properties.

Method: Thirty-two (32) Wistar rats were divided into four groups (A-D) of eight (8) rats each. Group A (Control) received 0.5 ml of Polysorbate 20; B received 10 mg/kg of BPA; C received 10 mg/kg BPA and 20 mg/kg of GA while D received 20 mg/kg GA alone for 21 days. Learning and memory, depression, motor function, exploratory activity and anxiety were assessed with Morris water maze, forced swim, hanging wire, open field and elevated plus maze tests respectively. Neuronal architecture across treatment groups were examined using Golgi and Nissl stains.

Results: There was no significant difference in the learning curve and spatial memory across all groups in the Morris water maze. However, a significant increase (p<0.05) in duration of immobility was observed in the BPA only group in the forced swim test while GA significantly reduced the duration of immobility. Furthermore, no significant difference was observed in grooming, freezing time, rearing, stretched-attend posture, total squares visited and the centre square duration in the open field test. The BPA only group exhibited a significant increase in the time and frequency of entry in the closed arms in the elevated plus maze, which reduced significantly in the GA + BPA group. Similarity in hanging latency was observed in the forelimb hanging wire test across the groups. Nissl and Golgi staining showed loss of neuronal cells and dendritic spines in the cerebellum, cerebrum and the hippocampus in the BPA alone which was restored in the GA treated groups.

Conclusion: Our results suggest that GA improved behavioral and neural dysfunction in BPA-induced neurotoxicity.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/gallic-acid-ameliorates-the-neurobehavioural-deficits-induced-by-bisphenol-a-bpa-in-wistar-rats/