Ascorbic acid and gallic acid mitigate behavioural deficits and loss of cerebellar myelin induced by Bisphenol-A in Wistar rats.

Abstract

BackgroundBisphenol-A (BPA) is a chemical component of plastics, polycarbonates, and epoxy resins making it an environmentally ubiquitous chemical. Its toxicity has been linked to several disorders including neurological disorders. Gallic acid (GA) and Ascorbic acid (AA) are both antioxidants that have been reported to have neuroprotective effects. We therefore investigated the neuroprotective effects of GA and AA on BPA-induced neurotoxicity. Forty-eight (48) Wistar rats were grouped into Control, BPA, BPA+AA, BPA+GA, AA, and GA groups with eight rats in each group. All treatments were administered via oral gavage for 21 days. Behavioral experiments were conducted to assess forelimb strength (hanging wire test), anxiety (open field and elevated plus maze tests), depression (forced swim test), and spatial memory (Morris water maze). Rats were perfused and brain samples were collected for Luxol fast blue staining. Sera were collected to evaluate the levels of inflammatory cytokines via Enzyme-Linked Immunosorbent Assay. ResultsThere was no significant difference in hanging latency between all the groups. There were also no significant changes in the open field test but the elevated plus maze showed an increase in time spent in closed arms in the BPA group indicative of anxiety. GA and AA reduced the duration of immobility that was elevated in the BPA group which suggests they have antidepressant-like effects. Additionally, we observed disruption in the Purkinje cell layer of the cerebellum in the BPA-alone group. ConclusionBPA seems to cause anxiety and depressive-like effects which are ameliorated by the gallic acid and ascorbic acid.