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Bisphenol A Exposure Induces Small Intestine Damage Through Oxidative Stress, Inflammation, and Microbiota Alteration in Rats
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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.
Bisphenol A (BPA), a widespread environmental contaminant used in plastics and resins, poses significant health risks due to its endocrine-disrupting properties and potential for inducing intestinal toxicity. This study explored the toxicological effects of BPA on the small intestine of rats, focusing on the duodenum, jejunum, and ileum. Histopathological evaluation revealed that the duodenum experienced the most severe structural damage, including villous atrophy, epithelial shedding, and mitochondrial degeneration. BPA exposure disrupted oxidative stress homeostasis by reducing superoxide dismutase activity and increasing malondialdehyde levels, along with upregulating antioxidant-related genes like GPX2 and HO-1 upregulated, indicating lipid peroxidation and oxidative damage. Inflammatory markers such as IL-1 and NFκB were significantly upregulated, highlighting an active inflammatory response and epithelial cell apoptosis. BPA also altered lipid metabolism, with increased expression of lipogenic genes such as SREBP-1c and FAS, indicating metabolic dysregulation. Fecal microbiota analysis revealed reduced α-diversity, enrichment of pathogenic taxa like Escherichia-Shigella, and depletion of beneficial genera such as Lachnospiraceae NK4A136 group, exacerbating gut inflammation and barrier dysfunction. These findings suggest that BPA-induced small intestinal damage is driven by oxidative stress, inflammation, and gut dysbiosis, with the duodenum and jejunum being the more vulnerable segments.
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Microplastics and Nanoplastics in the Gastrointestinal System: Mechanisms, Risks, and Therapeutic Opportunities
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Microplastics and nanoplastics accumulate in the gastrointestinal tract where they disrupt tight junction proteins, induce oxidative stress, promote gut dysbiosis, and activate inflammatory pathways linked to IBD, colorectal cancer, and IBS. Emerging mitigation strategies including probiotic-based approaches and polysaccharide binding agents offer potential therapeutic avenues for reducing GI microplastic burden and associated disease risk.
Microplastics and Nanoplastics in the Gastrointestinal System: Mechanisms, Risks, and Therapeutic Opportunities
AI summary Read the abstract
Microplastics and nanoplastics accumulate in the gastrointestinal tract where they disrupt tight junction proteins, induce oxidative stress, promote gut dysbiosis, and activate inflammatory pathways linked to IBD, colorectal cancer, and IBS. Emerging mitigation strategies including probiotic-based approaches and polysaccharide binding agents offer potential therapeutic avenues for reducing GI microplastic burden and associated disease risk.
Microplastics and Nanoplastics in the Gastrointestinal System: Mechanisms, Risks, and Therapeutic Opportunities
AI summary Read the abstract
Microplastics and nanoplastics accumulate in the gastrointestinal tract where they disrupt tight junction proteins, induce oxidative stress, promote gut dysbiosis, and activate inflammatory pathways linked to IBD, colorectal cancer, and IBS. Emerging mitigation strategies including probiotic-based approaches and polysaccharide binding agents offer potential therapeutic avenues for reducing GI microplastic burden and associated disease risk.
Polystyrene Microplastics and Bisphenol A Exposure Worsen Intestinal Injury in Diabetic Mice by Disrupting Gut Microbiota and Metabolites
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Researchers exposed diabetic mice to polystyrene microplastics and bisphenol A, then examined intestinal effects using metabolomics and gut microbiome sequencing. The study found that both pollutants worsened intestinal injury in diabetic mice by disrupting gut barrier proteins, altering beneficial metabolites like long-chain fatty acids, and shifting gut microbial composition toward less favorable species.
Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway
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Mice that swallowed polystyrene microplastics for 28 days developed oxidative stress and inflammation in their colons, leading to a weakened intestinal barrier with reduced protective mucus and loosened cell connections. The largest microplastics (5 micrometers) caused the most severe gut damage through a specific inflammatory pathway (NF-kB/NLRP3/MLCK), and antioxidant treatment was able to partially reverse the effects.
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