ESPE Abstracts

Background: The ever increasing uses of electronic gadgets are becoming a widespread source of Bisphenol-A accumulation. As studies have been reported that low level BPA accumulation may produce neurological effects but still limited studies have re-examined for its adverse effects in terms of acute exposure from electronic devices.

Objective and hypotheses: To investigate the effects of BPA on oxidative damage in terms of activity level of antioxidant enzymes in different regions of the rat brain.

Method: In this study, BPA migration was estimated through physio-chemical parameters and leachate (equivalent to 4 mg/kg body weight) was used for animal dosing. Three groups of Albino Wister rats (190±20 g) were used for control, sham, and treated. The antioxidant enzymes including superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GPx), and reduced glutathione level (GSH) were measured in different brain regions, i.e. corpus striatum, frontal cortex, thalamus, and midbrain.

Results: No significant changes were observed in most of the brain regions yet the level of GPx activity in corpus striatum (29.65±0.98 nmol/min per mg protein) and level of GSH activity in frontal cortex (2.33±0.12 μmol/g protein) was found to decrease significantly (P<0.05) when compared to controls. In addition, no significant effects were observed for the oxidative damage in brain regions of sham group when compared to control group.

Conclusion: Thus study suggests that acute exposure (4 mg/kg body weight per day up to 28 days) of BPA does not induce significant oxidative damage in the rat’s brain. Furthermore, study might re-examine before affirm the final remark for subscribers and regulatory bodies at similar doses.