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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
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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.
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Bisphenol S (BPS), widely used as a 'safer' substitute for BPA in plastics, caused oxidative stress and cell death in rainbow trout liver cells. The findings raise concerns that BPS—found in products marketed as BPA-free—may not be a safe alternative for fish health or for humans consuming contaminated seafood.
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Exposure to bisphenol A (BPA), a chemical found in many plastics and food-contact materials, was shown to cause structural damage to the small intestine in an animal model. The damage was linked to oxidative stress, where BPA triggered an imbalance between harmful reactive oxygen species and the body's antioxidant defenses. These findings add to growing evidence that BPA disrupts gastrointestinal health beyond its well-documented hormonal effects.
Bisphenols—A Threat to the Natural Environment
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This review examines the environmental and health threats posed by bisphenol A (BPA) and its replacements, bisphenol F and bisphenol S, which were introduced as safer alternatives. However, because these substitutes have similar chemical structures to BPA, they may pose comparable risks to human health and the environment, including hormone disruption. The study is relevant to microplastics research because bisphenols are common additives in plastics that can leach out as plastics break down into microparticles.
Is bisphenol A sorbed onto microplastics less bioavailable than freely dissolved bisphenol A? Implications for the gut health in a murine model
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Using an in vivo rat model, researchers tested whether bisphenol A adsorbed onto microplastics is less bioavailable in the gastrointestinal tract than freely dissolved BPA, finding that plastic-bound BPA showed altered absorption kinetics and different hormonal effects than dissolved BPA.
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This review presents evidence that BPS and BPF — chemicals used as 'BPA-free' replacements in plastics — have similar cancer-promoting and endocrine-disrupting properties to BPA itself. The substitution of one hormone-disrupting plastic chemical with nearly identical alternatives means consumers are not actually avoiding the health risks they are trying to escape.
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