Protective Effect of Naringin on Bisphenol Ainduced Cognitive Dysfunction and Oxidative Damage in Rats

<div style=textalign: justify;>bisphenol a (bpa) is one of the highest volume chemicals produced worldwide, which is used in many plastic industries. the present study aimed to evaluate the effect of bpa on cognitive functions and oxidative stress, and determine whether the naringin (ng) coadministration can modify the effect of this compound on cognitive functions and inhibit any possible oxidative stress in the brain tissue of rats. adult male wistar rats were divided into six groups. group i: control, group ii: bpatreated rats (50 mg/kg/day), group iii, iv, v: bpa+ng (40, 80, 160 mg/kg/day), group vi: ng (160 mg/kg/day) alone. cognitive functions were evaluated using stepdown latency (sdl) on a passive avoidance apparatus, and transfer latency (tl) in elevated plusmaze. a significant decrease in sdl, prolongation of tl, noticeable oxidative impairment and increase in acetylcholinesterase activity were observed in the bpatreated in comparison with the control group. also, the coadministration of ng (160 mg/kg) antagonized the effect of bpa on sdl and tl, attenuated oxidative damage by lowering malondialdehyde and nitrite concentrations and restored superoxide dismutase, catalase, and glutathione stransferase activities. on the other hand, acetylcholinesterase activity was reduced in the groups coadministred with ng (80 or 160 mg/kg) and bpa in comparison with the bpa alonetreated group. the present study highlighted the therapeutic potential of ng against bpainduced cognitive impairment and oxidative damage.</div>