Gallic acid protects rat liver mitochondria ex vivo from bisphenol A induced oxidative stress mediated damages

Humans are often exposed to bisphenol A (BPA), the monomer of polycarbonate plastics and epoxy resins, through BPA contaminated drinking water, beverages and foods, packaged in polycarbonate plastic bottles and cans coated with epoxy resins due to leaching. Several research groups have reported that BPA may cause damage of mitochondria in liver, kidney, heart and brain cells by inducing oxidative stress. The antioxidant efficacy of gallic acid (GA), a polyphenol compound obtained from plants, against different toxicants induced oxidative stress has been well established. The aim of the present study was to examine the protective efficacy of GA against BPA induced oxidative damages of the rat liver mitochondria ex vivo. In our study, we have found a significant decrease in the intactness of mitochondria; a significant increase (P <= 0.001) in the levels of lipid peroxidation end product (i.e. malondialdehyde) and protein carbonylation product; and also a significant decrease (P <= 0.001) in the reduced glutathione content; when mitochondria were incubated with BPA (160 mu M/ ml) only. These results indicate that BPA probably causes damage to the cellular macromolecules through oxidative stress. We have observed significant counteractions (P <= 0.001) against BPA induced alterations in mitochondrial intactness, lipid peroxidation and protein carbonylation products formation and reduced glutathione content when mitochondria were incubated with BPA and GA (20 mu g/ml/ 40 mu g/ml/ 80 mu g/ml) in combination in a dose-dependent manner. Gallic acid also showed significant restorations (P <= 0.001) of the activities of antioxidant enzymes, Krebs cycle enzymes, respiratory chain enzymes and thiolase when mitochondria were incubated with BPA and dosage of GA (20 mu g/ml/ 40 mu g/ml/ 80 mu g/ml) in combination compared to BPA incubated mitochondria. Furthermore, GA significantly (P <= 0.001) counteracted the BPA induced decrease in tryptophan and NADH auto-fluroscence levels in mitochondria. This result suggests that GA protects the mitochondria probably by reducing the oxidative stress. Besides, GA protects the mitochondrial surface from BPA induced oxidative damages as viewed under the scanning electron microscope. Considering all the results, it can be concluded that GA shows potent efficacy in protecting the rat liver mitochondria ex vivo from BPA induced oxidative stress mediated damages.