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In vivo methylmercury toxicity is exacerbated by polystyrene microplastic exposure, leading to colon barrier disruption, gut dysbiosis, and systemic oxidative imbalance
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Researchers co-exposed rats to environmentally relevant doses of methylmercury and 5-µm polystyrene microplastics for eight weeks, finding that combined exposure caused greater gut barrier disruption, dysbiosis, oxidative stress, and systemic inflammation than either contaminant alone — with the intestine emerging as an early and sensitive target.
Methylmercury (MeHg) is a well-recognized toxicant, whereas microplastics (MP) are contaminants whose health effects continue to be explored. Evidence suggests that concomitant exposure to MeHg and polystyrene (PS) may enhance adverse outcomes in the gastrointestinal system. The aim of this study was to investigate the combined effects of MeHg and PS-MP on intestinal homeostasis, as well as systemic oxidative and inflammatory responses. A total of 64 rats with 30-days-old (n = 16 per group) were exposed to environmentally relevant doses of 0.5 mg/L MeHg and/or 0.2 mg/L PS-MP of 5 µm during 8 weeks. Co-exposure resulted in colon shortening, mucus depletion, and disruption of tight junction proteins, accompanied by macrophage infiltration and elevated pro-inflammatory cytokines. Structural and inflammatory changes were accompanied by gut dysbiosis, including altered microbial composition and reduced diversity indices. Biochemically, co-exposure amplified oxidative stress in the colon, with loss of free thiols and enhanced lipid peroxidation, while not markedly affecting glutathione-S-transferase activity. Systemically, combined treatment increased serum cytokines and induced genotoxicity. Although compensatory antioxidant responses were detected in blood, oxidative stress was evident in peripheral organs, particularly liver, kidneys, and heart. Taken together, these findings demonstrate that the intestine may be an early and sensitive target following co-exposure to MeHg and PS-MP, driving cytokine release into circulation and contributing to systemic injury. Our study provides novel in vivo evidence that combined PS-MP and MeHg exposure exacerbates some biological outcomes noted with individual contaminant exposure, indicating the importance of considering co-contamination scenarios in risk assessment of emerging pollutants.
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In vivo methylmercury toxicity is exacerbated by polystyrene microplastic exposure, leading to colon barrier disruption, gut dysbiosis, and systemic oxidative imbalance
AI summary Read the abstract
Researchers co-exposed rats to environmentally relevant doses of methylmercury and polystyrene microplastics for eight weeks and found synergistic damage to the colon — including tight junction breakdown, gut dysbiosis, and amplified oxidative stress — with systemic cytokine release propagating injury to the liver, kidneys, and heart beyond what either contaminant caused alone.
In vivo methylmercury toxicity is exacerbated by polystyrene microplastic exposure, leading to colon barrier disruption, gut dysbiosis, and systemic oxidative imbalance
AI summary Read the abstract
Researchers found that co-exposure to polystyrene microplastics and methylmercury worsens biological harm beyond what either contaminant causes alone, disrupting the colon barrier, destabilizing gut microbiota, and triggering systemic oxidative imbalance — underscoring the importance of studying pollutant mixtures rather than individual contaminants in isolation.
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Researchers found that polystyrene microplastic exposure worsened intestinal barrier dysfunction in mice on high-fat diets, with the combination of obesity and microplastic exposure producing greater gut permeability and inflammation than either factor alone, suggesting compounding risks in metabolically vulnerable individuals.
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Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
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