News | Can microplastics enter semen? Study reveals they trigger a "self-destruct program" in testicular cells
In a study that has drawn global attention, scientists from a Chongqing, China team discovered that microplastics (MPs) released from everyday plastic tableware not only enter the human body but can also be detected in semen, and in animal experiments trigger "autophagy and apoptosis responses" in testicular cells, leading to significant declines in sperm count and motility. The study is the first to reveal the molecular mechanism by which microplastics induce germ cell stress and self-destruction through the FOXA1/MAP3K1/p38 signaling pathway, providing key clues to potential environmental factors in male infertility.
Microplastics and male infertility: a hidden environmental threat
About half of infertility cases worldwide are related to male factors, and sperm counts are declining at a rate of approximately 1–2.6% per year. In addition to lifestyle influences such as obesity and stress, environmental pollutants, especially microplastic exposure, are becoming an overlooked source of risk. Polystyrene (PS) and polyvinyl chloride (PVC) fragments released from disposable plastic tableware often enter the human body through food or drinking water. Animal studies have shown that these particles can induce oxidative stress, hormonal disruption, and testicular damage, but direct evidence of their mechanism of action in the human reproductive system remains lacking.
Study design: multi-level validation from human semen to animal models
The study was published in the Journal of Nanobiotechnology. The team analyzed semen samples from 200 men of reproductive age (mean age 24.6 years) at the Chongqing Human Sperm Bank between 2020 and 2021, and recorded their lifestyle, BMI, and frequency of plastic tableware use. Samples were freeze-dried, enzymatically digested, and analyzed by infrared microscopy to detect the types and quantities of microplastics.
The results showed that microplastics were detected in 55.5% (111/200) of samples, with a total of 128 particles. The main polymers were PVC (36.7%) and PS (32.0%), followed by polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP). Those who used plastic tableware daily had significantly higher microplastic concentrations in their semen (p < 0.05).
In in vitro and animal experiments, researchers administered 50 nanometer-sized PS microplastics orally to mice for 8 consecutive weeks. The results showed that sperm concentration decreased by 33%, total motility decreased by 21%, and progressive motility decreased by 38%, accompanied by structural disorganization of testicular tissue and massive accumulation of autophagosomes.
Molecular mechanism: the FOXA1/MAP3K1/p38 signaling axis triggers autophagy and apoptosis
Transcriptome sequencing revealed that a total of 985 differentially expressed genes were significantly enriched in autophagy and apoptosis pathways. Key autophagy genes ATG5, ATG7, and BECN1 were significantly upregulated, and the autophagy marker proteins LC3β and p62/SQSTM1 increased by 69% and 138%, respectively. Meanwhile, pro-apoptotic proteins Bax and Bad were upregulated, while anti-apoptotic proteins Bcl-2 and Bcl-xL decreased, and cleavage levels of Caspase-3 and Caspase-9 increased.
Further mechanistic analysis revealed that PS microplastics can activate the MAPK cascade—MAP3K1 promotes p38 phosphorylation, which in turn activates the downstream transcription factor c-fos; while the transcription factor FOXA1 directly binds to the MAP3K1 promoter and interacts with its protein, thereby initiating the entire signaling cascade. After applying the p38 inhibitor Adezmapimod or knocking down the FOXA1 gene, the above autophagy and apoptosis responses were significantly suppressed, confirming that the FOXA1/MAP3K1/p38/c-fos axis plays a central role in microplastic-induced reproductive damage.
Human findings and public health implications
At the population level, although the study did not find significant correlations in the overall sample, among individuals with low BMI and those who frequently used plastic tableware, microplastic content showed a marginal negative correlation with sperm concentration (p = 0.07–0.08), suggesting that certain populations may be more susceptible.
The research team noted that this is the first study to simultaneously integrate human epidemiological data with cellular and animal mechanistic evidence, demonstrating that microplastics derived from plastic tableware are not "inert" pollutants, but may directly impair spermatogenesis through the autophagy-apoptosis pathway.
Although the authors emphasized that limitations remain—such as animal experimental doses being higher than environmental exposure levels and actual fertility outcomes not being assessed—the study provides a solid foundation for understanding the relationship between microplastics and male reproductive disorders.
Conclusion
This study reveals the potential threat of plastic tableware use and microplastic exposure to the male reproductive system, particularly in low-body-weight and high-exposure populations. The study indicates that 50 nanometer-sized PS microplastics can trigger autophagy and apoptosis in testicular cells by activating the FOXA1/MAP3K1/p38 signaling pathway, thereby impairing sperm count and motility.
The researchers call for stricter public health policies to limit microplastic release from food containers and to promote the use of safe alternative materials.
Notícias | Microplásticos podem entrar no sêmen? Estudo mostra que eles ativam um ‘programa de autodestruição’ nas células testiculares
News | Can microplastics enter semen? Study reveals they trigger a "self-destruct program" in testicular cells
In a study that has drawn global attention, scientists from a Chongqing, China team discovered that microplastics (MPs) released from everyday plastic tableware not only enter the human body but can also be detected in semen, and in animal experiments trigger "autophagy and apoptosis responses" in testicular cells, leading to significant declines in sperm count and motility. The study is the first to reveal the molecular mechanism by which microplastics induce germ cell stress and self-destruction through the FOXA1/MAP3K1/p38 signaling pathway, providing key clues to potential environmental factors in male infertility.
Microplastics and male infertility: a hidden environmental threat
About half of infertility cases worldwide are related to male factors, and sperm counts are declining at a rate of approximately 1–2.6% per year. In addition to lifestyle influences such as obesity and stress, environmental pollutants, especially microplastic exposure, are becoming an overlooked source of risk. Polystyrene (PS) and polyvinyl chloride (PVC) fragments released from disposable plastic tableware often enter the human body through food or drinking water. Animal studies have shown that these particles can induce oxidative stress, hormonal disruption, and testicular damage, but direct evidence of their mechanism of action in the human reproductive system remains lacking.
Study design: multi-level validation from human semen to animal models
The study was published in the Journal of Nanobiotechnology. The team analyzed semen samples from 200 men of reproductive age (mean age 24.6 years) at the Chongqing Human Sperm Bank between 2020 and 2021, and recorded their lifestyle, BMI, and frequency of plastic tableware use. Samples were freeze-dried, enzymatically digested, and analyzed by infrared microscopy to detect the types and quantities of microplastics.
The results showed that microplastics were detected in 55.5% (111/200) of samples, with a total of 128 particles. The main polymers were PVC (36.7%) and PS (32.0%), followed by polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP). Those who used plastic tableware daily had significantly higher microplastic concentrations in their semen (p < 0.05).
In in vitro and animal experiments, researchers administered 50 nanometer-sized PS microplastics orally to mice for 8 consecutive weeks. The results showed that sperm concentration decreased by 33%, total motility decreased by 21%, and progressive motility decreased by 38%, accompanied by structural disorganization of testicular tissue and massive accumulation of autophagosomes.
Molecular mechanism: the FOXA1/MAP3K1/p38 signaling axis triggers autophagy and apoptosis
Transcriptome sequencing revealed that a total of 985 differentially expressed genes were significantly enriched in autophagy and apoptosis pathways. Key autophagy genes ATG5, ATG7, and BECN1 were significantly upregulated, and the autophagy marker proteins LC3β and p62/SQSTM1 increased by 69% and 138%, respectively. Meanwhile, pro-apoptotic proteins Bax and Bad were upregulated, while anti-apoptotic proteins Bcl-2 and Bcl-xL decreased, and cleavage levels of Caspase-3 and Caspase-9 increased.
Further mechanistic analysis revealed that PS microplastics can activate the MAPK cascade—MAP3K1 promotes p38 phosphorylation, which in turn activates the downstream transcription factor c-fos; while the transcription factor FOXA1 directly binds to the MAP3K1 promoter and interacts with its protein, thereby initiating the entire signaling cascade. After applying the p38 inhibitor Adezmapimod or knocking down the FOXA1 gene, the above autophagy and apoptosis responses were significantly suppressed, confirming that the FOXA1/MAP3K1/p38/c-fos axis plays a central role in microplastic-induced reproductive damage.
Human findings and public health implications
At the population level, although the study did not find significant correlations in the overall sample, among individuals with low BMI and those who frequently used plastic tableware, microplastic content showed a marginal negative correlation with sperm concentration (p = 0.07–0.08), suggesting that certain populations may be more susceptible.
The research team noted that this is the first study to simultaneously integrate human epidemiological data with cellular and animal mechanistic evidence, demonstrating that microplastics derived from plastic tableware are not "inert" pollutants, but may directly impair spermatogenesis through the autophagy-apoptosis pathway.
Although the authors emphasized that limitations remain—such as animal experimental doses being higher than environmental exposure levels and actual fertility outcomes not being assessed—the study provides a solid foundation for understanding the relationship between microplastics and male reproductive disorders.
Conclusion
This study reveals the potential threat of plastic tableware use and microplastic exposure to the male reproductive system, particularly in low-body-weight and high-exposure populations. The study indicates that 50 nanometer-sized PS microplastics can trigger autophagy and apoptosis in testicular cells by activating the FOXA1/MAP3K1/p38 signaling pathway, thereby impairing sperm count and motility.
The researchers call for stricter public health policies to limit microplastic release from food containers and to promote the use of safe alternative materials.
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Collected from the internet