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Evaluation of polyethylene microplastics toxicity using Nrf2/ARE and MAPK/Nrf2 signaling pathways
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Researchers exposed male and female rats to varying doses of polyethylene microplastics and found dose-dependent increases in oxidative stress markers and disruptions to reproductive hormone levels. They identified specific cellular signaling pathways, including the Nrf2 antioxidant response system, that were affected by microplastic exposure. The study suggests that microplastic ingestion may trigger oxidative damage and reproductive effects through identifiable molecular mechanisms.
Microplastics (MPs) have emerged as a serious global environmental threat due to their resistance to degradation and persistence in ecosystems. Given their potential risks to human health, it is essential to thoroughly investigate the mechanisms of toxicity and associated health consequences. This study examined the toxicological and reproductive effects of varying doses of polyethylene microplastics (PE-MPs) in 120 male and female Sprague Dawley rats. A statistically significant, dose-dependent increase in malondialdehyde levels was observed, along with a reduction in catalase activity. Furthermore, alterations were detected in sexual hormone levels and disruptions were noted in both the Kelch-like ECH-associated protein 1 (Keap1)-Nrf2-ARE (antioxidant response element) and p38 MAPK-Nrf2 signaling pathways. PE-MP exposure also produced marked histopathological changes in the testes and ovaries. These findings indicate that reproductive toxicity from PE-MPs is associated with impairments in the Keap1-Nrf2-ARE and p38 MAPK-Nrf2 pathways. The results underscore the importance of limiting MP exposure to mitigate potential health hazards and provide new data on the potential mechanisms of toxicity of MPs.
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Polystyrene microplastics induce blood–testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats
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Researchers fed rats polystyrene microplastics for 90 days and found significant damage to male reproductive health, including reduced sperm quality, damaged sperm-producing tissue, and increased cell death. The study identified a specific molecular pathway where microplastics triggered oxidative stress that disrupted the blood-testis barrier, a critical protective structure in the testes. These findings provide new evidence that microplastic exposure may pose risks to male reproductive function.
Polystyrene microplastics induce blood-testis barrier disruption regulated by MAPK-Nrf2 signaling pathway in rats
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Researchers found that polystyrene microplastics (PS-MPs) disrupted the blood-testis barrier in male rats after 90 days of exposure, with higher doses (0.15 and 1.5 mg/d) causing significant spermatogenic cell apoptosis and reduced sperm motility through activation of the MAPK-Nrf2 signaling pathway.
Developmental and reproductive toxic effects of exposure to microplastics: A review of associated signaling pathways
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This review examines how microplastic exposure affects reproductive and developmental health across multiple species, focusing on the biological signaling pathways involved. Researchers found that microplastics can trigger oxidative stress, inflammation, and hormonal disruption through specific cellular pathways, leading to reduced fertility and abnormal development. The study provides a molecular-level framework for understanding why microplastics may pose risks to reproductive health.
Mitigative potential of kaempferide against polyethylene microplastics induced testicular damage by activating Nrf-2/Keap-1 pathway
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Researchers tested whether kaempferide, a natural plant compound with antioxidant properties, could protect against testicular damage caused by polyethylene microplastics in rats. They found that the microplastics triggered significant oxidative stress and tissue damage in the testes, but kaempferide treatment substantially reduced these harmful effects by activating a key protective cellular pathway. The study suggests that natural antioxidant compounds may help counteract some of the reproductive harm associated with microplastic exposure.
Adverse effects of microplastics and oxidative stress-induced MAPK/Nrf2 pathway-mediated defense mechanisms in the marine copepod Paracyclopina nana
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Researchers studied how nano- and micro-sized polystyrene particles affect a tiny marine crustacean called a copepod at the molecular level. They found that the smallest particles caused the most severe oxidative stress and triggered cellular defense pathways, with effects worsening at higher concentrations. The study suggests that microplastics can disrupt the internal chemistry of marine organisms even at sizes too small to see with the naked eye.
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