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Polystyrene nanoplastics exposure induces reproductive toxicity in male mice associated with the gut-liver/testis axis.
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In a study, male mice that ate tiny plastic particles (nanoplastics, like those found in bottled water and packaged food) for 28 days showed weight loss, disrupted gut bacteria, liver stress, and lower-quality sperm. The findings suggest these plastic particles may harm male fertility partly by throwing off the gut's healthy bacteria, which then seems to send disruptive signals to the liver and testes. This is animal research, not proof of the same effect in humans, but it adds to growing concerns about how the microplastics we're constantly exposed to might affect long-term reproductive health.
Environmental nanoplastics are increasingly prevalent in global environments and represent an emerging systemic health risk, yet the mechanistic links between nanoplastic exposure and multi-organ dysfunction in mammals remain incompletely characterized. We integrated phenotypic assessments, gut shotgun metagenomics, and dual-organ transcriptomics to investigate the toxic effects of 28-day oral exposure to polystyrene nanoplastics (PS-NPs) in male CD-1 mice. PS-NPs induced a non-monotonic dose-dependent response, characterized by significant body weight loss at high doses, severe impairment of sperm motility, and progressive epididymal histopathological lesions. Gut metagenomics revealed significant microbiota dysbiosis, including an elevated Firmicutes/Bacteroidota ratio and marked depletion of beneficial commensal bacteria such as Ligilactobacillus murinus. Hepatic transcriptomics identified dysregulation of metabolic, detoxification, and circadian rhythm pathways, while testicular transcriptomics identified sustained transcriptional downregulation of genes annotated to steroid hormone biosynthesis and alterations in FoxO and apoptosis-related signaling. Spearman correlation network analysis identified associations between specific microbial shifts and organ-specific transcriptional alterations, providing a hypothesis-generating framework for the proposed gut-liver/testis axis. Together, these findings indicate that, under the present experimental conditions, oral PS-NPs exposure was associated with gut microbial dysbiosis, hepatic transcriptional perturbations, reduced sperm motility, and epididymal histopathological alterations, while the mechanistic relationships among these changes require further experimental validation.
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Scientists exposed mice to polypropylene microplastics (found in many plastic food containers and packaging) for five weeks and found changes to gut bacteria, including a drop in a helpful probiotic species, along with shifts in genes affecting testicle function, though hormone levels and organ weights stayed normal. This suggests microplastics might disrupt the gut-reproductive system connection before causing obvious physical damage, but since this was only in mice, more research is needed to know what it means for human fertility.
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Scientists found that tiny plastic particles (nanoplastics, from the breakdown of everyday plastics) damaged the guts of male guppies, making it harder for them to digest food and absorb nutrients. This gut damage triggered a chain reaction—lowering testosterone, weakening sperm, and ultimately causing complete reproductive failure at the highest exposure level tested. While this study was done in fish, it raises important questions about how nanoplastics—which are already found in human blood and organs—might similarly affect gut health and fertility in people, an area that needs more research.
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