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Effects of polystyrene microparticles exposures on spermatogenic cell differentiation and reproductive endpoints in male mice
Summary
Researchers found that very small polystyrene microplastics (0.1 micrometers) accumulated in mouse testicular tissue and sperm-producing cells, leading to reduced sperm quality and impaired reproductive function. The particles triggered oxidative stress and disrupted the normal process of sperm cell development. This study adds to growing evidence that microplastic exposure could contribute to male fertility problems in humans, particularly from the smallest particles that can penetrate reproductive tissues.
The widespread distribution of microplastics in the environment has raised concerns about their potential implications for human health. Microplastics accumulate in animals and humans, but the risks associated with these pollutants are not fully understood. This study aimed to investigate the effects of polystyrene microplastics on the male reproductive system. The 0.1 μm polystyrene (PS) could accumulate in the testicular tissue and spermatogonia GC-1, while 1 μm PS was not easy to enter and accumulate in the testicular tissue and cells. Mice continuously exposed for 3-months to 0.1 μm PS demonstrated lower fertility and inhibited spermatogonium differentiation compared to control mice. The 0.1 μm PS were dispersed throughout the seminiferous tubule of the testis. Metabolic reprogramming was found to be involved in these processes. Histone methylation and autophagy-related pathways showed significant differences following PS treatment in testis tissue and GC-1 cells. Our findings suggest that chronic exposure to 0.1 μm PS inhibited spermatogenic cell differentiation and impaired fertility in male mice. We propose that abnormal epigenetic modifications in 0.1 μm PS exposed mice contributed to the dysregulation of glycolytic enzymes, and that the impaired autophagic pathway exacerbated the accumulation of glycolytic enzymes further. Glycolysis plays a critical role in the regulation of spermatogenic cell differentiation, and its regulation partially alleviated the impairments associated with PS exposure. In conclusion, our findings suggest that chronic exposure to nanoplastics PS inhibited spermatogenic cell differentiation and impaired fertility in male mice via disrupted epigenetic modification and metabolic dysregulation.