Over the last decade, microplastics and nanoplastics (NPs) have emerged as a global concern. Our former world seems to be normalizing the plastic usage to the extent of little particles accumulating in human bodies. Among these, nanoplastics, which are particles smaller than one micrometer, have been identified as particularly concerning contaminants. Polyethylene is one of the most commonly used plastics that is used in countless applications, such as in food packaging, and is often overlooked. Most people are unaware that the waxy coating on the surface of their “paper” cups is also made of low-density polyethylene.
A new study performed by Jiaqi Sun and his colleagues examined the effects of orally ingested NPs on the male reproductive system and intergenerational genetics. The research team used the male C57BL/6J (F0 generation) model mice. They have been given 200 nm of polyethylene nanoparticles (PE-NPs)s orally at a concentration of 2 mg/L daily for 35 days. The dosage of the NPs was relevant due to the similarity between the concentration that has been detected in human blood. These mice (F0 generation) were then bred and produced offspring (F1 generation). The new generation was never directly exposed to the NP; however, the researchers observed proof of reproductive disruption and damaged testicles in both generations. This suggests that the harm of NP exposure can be passed along the male lineage.
To examine the mechanisms behind this inheritance, the team performed qRT-PCR and miRNA-sequencing techniques. They have analyzed the expression of genes that are responsible for endoplasmic reticulum stress. In addition, by using histological staining and hormonal assays, and a computer-assisted sperm analysis (CASA) system, they have assessed sperm count, motility, and histological abnormalities.
To uncover the underlying intergenerational effects, the research team investigated sperm quality, mobility, and hormone levels. The sperm collected from the PE-NP exposed male mice had increased histological abnormalities, while it had a decrease in count and motility. The results were the same for the male offspring. Testicular tissue in both F0 and F1 generations had shown signs of a significant loss of spermatogenic cells, vacuolization, and atrophied seminiferous tubules. Hormone analysis exhibited reductions in 11-ketotestosterone and testosterone levels.
Results showed the upregulation of the ER stress markers like BIP, IRE1α, XBP1s, CHOP, and JNK, and apoptotic regulators Bax and Bcl-1. Genes that play a role in testosterone synthesis and sperm development, such as Insl3, SYCP3, and StAR, were downregulated. Exposure to PE-NPs caused alterations in the sperm miRNA levels, especially decreasing miR-122-5p, miR-5100, and miR-6240 while increasing miR-1983. These miRNA signatures were detected not only in the F1 offspring but fecal microbiota transplantation (FMT) studies.
In the FMT trials, the fecal material from the F0 generation male mice was transferred to germ-free mice, resulting in reproductive impairments. These results strongly indicate that the gut microbial disturbances play a role. Gut microbiota sequencing further confirmed that PE-NP exposure perturbed microbial composition. The perturbation included the increased number of potentially harmful Desulfovibrio and Ruminococcus gnavus, alongside a reduction in beneficial bacteria such as Allobaculum. These microbial shifts were analytically linked to gene expression alteration related to sperm and hormone production.
In conclusion, the study highlights how paternal exposure to PE-NPs can cause heritable reproductive toxicity through a mechanism that involves both sperm miRNA and gut microbiota imbalance. These findings not only raise important questions on how environmental plastic exposure affects public reproductive health and fertility, but also encourage further exploration of miRNA and microbiota as potential therapeutic targets.
Author: Sude Aras
Editor: Simten Gönentür
Reference: Pu, R., Sun, X., & Zhang, A. (2025). Comment on “MicroRNA and gut microbiota alter intergenerational effects of paternal exposure to polyethylene nanoplastics.” ACS Nano, 19(27), 24143–24145. https://doi.org/10.1021/acsnano.5c06523
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