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Bisphenol S (BPS) Alters Xanthine Oxidoreductase Activity to Elevate Oxidative Stress Mediated Protein Carbonylation in Small Intestine of Rat ex vivo
Summary
Bisphenol S (BPS), a replacement for the now-restricted bisphenol A commonly leached from food packaging plastics, was found to increase protein carbonylation and alter the xanthine oxidoreductase enzyme system in rat intestinal tissue, generating oxidative stress in a dose-dependent manner. This suggests that BPS is not a safe substitute for BPA and that plastics labeled as BPA-free may still pose significant chemical hazards to the digestive system.
Bisphenol S (BPS) is a replacement bisphenol used instead of bisphenol A (BPA) to manufacture polycarbonate plastics, epoxy resins, and thermal papers utilized in storage and packaging of foodstuffs, beverages and drinking water.Consequently, leaching of BPS from the food contact materials into the comestibles, followed by absorption of BPS-tainted comestibles by small intestine becomes the predominant source of BPS contamination to humankind.Though, BPS is known to elevate oxidative stress, its effects on xanthine oxidoreductase (XOR) system mediated oxidative induction of proteins remains unexplored.Therefore, the present study aims to evaluate the effect of BPS on oxidation of proteins by involving XOR system in small intestine of male albino rats ex vivo.BPS exposure has been found to significantly (P 0.001) increase protein carbonylation; alter the activities of XOR system by augmenting the activities of cytosolic and mitochondrial xanthine oxidase (XO) and cytosolic xanthine dehydrogenase; and diminish the concentrations of cytosolic and mitochondrial nitrite in a dose dependent manner compared to the control group.These results indicate that BPS elevates protein carbonylation and diminishes nitrite concentration probably by XOR system mediated oxidative stress generation in mammalian small intestine.