News | Can Microplastics Enter Semen? Study Shows They Trigger a ‘Self-Destruct Program’ in Testicular Cells
In a study that drew global attention, scientists from Chongqing, China, found that microplastics (MPs) released by everyday plastic tableware can enter the body and be detected in semen. In animal experiments, they triggered autophagy and apoptosis in testicular cells, significantly reducing sperm count and motility. For the first time, the study identified the molecular mechanism by which microplastics induce germ-cell stress and self-destruction through the FOXA1/MAP3K1/p38 signaling pathway, providing important clues to a potential environmental factor in male infertility.
Microplastics and Male Infertility: A Hidden Environmental Threat
Male factors are involved in about half of infertility cases worldwide, while sperm counts are declining by about 1–2.6% per year. Beyond lifestyle factors such as obesity and stress, environmental pollutants—especially microplastic exposure—are emerging as an overlooked risk. Polystyrene (PS) and polyvinyl chloride (PVC) fragments released by disposable plastic tableware commonly enter the body through food or drinking water. Animal studies show that these particles induce oxidative stress, hormonal disruption, and testicular damage, but direct evidence of their mechanism in the human reproductive system remains limited.
Study Design: Multilevel Validation From Human Semen to Animal Models
Published in the Journal of Nanobiotechnology, the study analyzed semen samples from 200 reproductive-age men at the Chongqing Human Sperm Bank between 2020 and 2021, with a mean age of 24.6 years. The team recorded lifestyle, BMI, and frequency of plastic tableware use. Samples underwent freeze-drying, enzymatic digestion, and infrared microscopy to identify and count microplastics.
Microplastics were detected in 55.5% (111/200) of samples, totaling 128 particles. The main polymers were PVC (36.7%) and PS (32.0%), followed by polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP). Men who used plastic tableware daily had significantly higher microplastic concentrations in semen (p < 0.05).
In vitro and animal experiments exposed mice orally to 50-nanometer PS microplastics for 8 consecutive weeks. Sperm concentration fell 33%, total motility fell 21%, and progressive motility fell 38%, accompanied by disrupted testicular tissue structure and substantial autophagosome accumulation.
Molecular Mechanism: The FOXA1/MAP3K1/p38 Signaling Axis Triggers Autophagy and Apoptosis
Transcriptome sequencing found 985 differentially expressed genes significantly enriched in autophagy and apoptosis pathways. Key autophagy genes ATG5, ATG7, and BECN1 were significantly upregulated, while the autophagy marker proteins LC3β and p62/SQSTM1 increased by 69% and 138%, respectively. Pro-apoptotic proteins Bax and Bad increased, anti-apoptotic proteins Bcl-2 and Bcl-xL decreased, and cleavage of Caspase-3 and Caspase-9 increased.
Further analysis showed that PS microplastics activate the MAPK cascade: MAP3K1 promotes p38 phosphorylation, which activates the downstream transcription factor c-fos. FOXA1 binds directly to the MAP3K1 promoter and interacts with its protein, initiating the entire cascade. The p38 inhibitor Adezmapimod or FOXA1 gene knockdown significantly suppressed autophagy and apoptosis, confirming the central role of the FOXA1/MAP3K1/p38/c-fos axis in microplastic-induced reproductive damage.
Human Findings and Public Health Significance
Although the overall human sample showed no significant association, microplastic levels had a borderline negative correlation with sperm concentration among people with low BMI and frequent plastic tableware use (p = 0.07–0.08), suggesting that certain groups may be more vulnerable.
The team said this was the first study to integrate human epidemiological data with cellular and animal mechanistic evidence. It suggests that microplastics from plastic tableware are not ‘inert’ pollution and may directly impair sperm production through cellular autophagy and apoptosis.
The authors noted limitations, including animal doses above environmental exposure levels and the lack of actual fertility outcomes. Even so, the study provides a strong basis for understanding the relationship between microplastics and impaired male fertility.
Conclusion
The study identified a potential threat to the male reproductive system from plastic tableware use and microplastic exposure, particularly among people with low body weight or high exposure. It found that 50-nanometer PS microplastics activate the FOXA1/MAP3K1/p38 pathway, causing autophagy and apoptosis in testicular cells and impairing sperm count and motility.
The researchers called for stricter public health policies to limit microplastic release from food containers and encourage safer alternative materials.
News | Can Microplastics Enter Semen? Study Shows They Trigger a ‘Self-Destruct Program’ in Testicular Cells
News | Can Microplastics Enter Semen? Study Shows They Trigger a ‘Self-Destruct Program’ in Testicular Cells
In a study that drew global attention, scientists from Chongqing, China, found that microplastics (MPs) released by everyday plastic tableware can enter the body and be detected in semen. In animal experiments, they triggered autophagy and apoptosis in testicular cells, significantly reducing sperm count and motility. For the first time, the study identified the molecular mechanism by which microplastics induce germ-cell stress and self-destruction through the FOXA1/MAP3K1/p38 signaling pathway, providing important clues to a potential environmental factor in male infertility.
Microplastics and Male Infertility: A Hidden Environmental Threat
Male factors are involved in about half of infertility cases worldwide, while sperm counts are declining by about 1–2.6% per year. Beyond lifestyle factors such as obesity and stress, environmental pollutants—especially microplastic exposure—are emerging as an overlooked risk. Polystyrene (PS) and polyvinyl chloride (PVC) fragments released by disposable plastic tableware commonly enter the body through food or drinking water. Animal studies show that these particles induce oxidative stress, hormonal disruption, and testicular damage, but direct evidence of their mechanism in the human reproductive system remains limited.
Study Design: Multilevel Validation From Human Semen to Animal Models
Published in the Journal of Nanobiotechnology, the study analyzed semen samples from 200 reproductive-age men at the Chongqing Human Sperm Bank between 2020 and 2021, with a mean age of 24.6 years. The team recorded lifestyle, BMI, and frequency of plastic tableware use. Samples underwent freeze-drying, enzymatic digestion, and infrared microscopy to identify and count microplastics.
Microplastics were detected in 55.5% (111/200) of samples, totaling 128 particles. The main polymers were PVC (36.7%) and PS (32.0%), followed by polyethylene (PE), polyethylene terephthalate (PET), and polypropylene (PP). Men who used plastic tableware daily had significantly higher microplastic concentrations in semen (p < 0.05).
In vitro and animal experiments exposed mice orally to 50-nanometer PS microplastics for 8 consecutive weeks. Sperm concentration fell 33%, total motility fell 21%, and progressive motility fell 38%, accompanied by disrupted testicular tissue structure and substantial autophagosome accumulation.
Molecular Mechanism: The FOXA1/MAP3K1/p38 Signaling Axis Triggers Autophagy and Apoptosis
Transcriptome sequencing found 985 differentially expressed genes significantly enriched in autophagy and apoptosis pathways. Key autophagy genes ATG5, ATG7, and BECN1 were significantly upregulated, while the autophagy marker proteins LC3β and p62/SQSTM1 increased by 69% and 138%, respectively. Pro-apoptotic proteins Bax and Bad increased, anti-apoptotic proteins Bcl-2 and Bcl-xL decreased, and cleavage of Caspase-3 and Caspase-9 increased.
Further analysis showed that PS microplastics activate the MAPK cascade: MAP3K1 promotes p38 phosphorylation, which activates the downstream transcription factor c-fos. FOXA1 binds directly to the MAP3K1 promoter and interacts with its protein, initiating the entire cascade. The p38 inhibitor Adezmapimod or FOXA1 gene knockdown significantly suppressed autophagy and apoptosis, confirming the central role of the FOXA1/MAP3K1/p38/c-fos axis in microplastic-induced reproductive damage.
Human Findings and Public Health Significance
Although the overall human sample showed no significant association, microplastic levels had a borderline negative correlation with sperm concentration among people with low BMI and frequent plastic tableware use (p = 0.07–0.08), suggesting that certain groups may be more vulnerable.
The team said this was the first study to integrate human epidemiological data with cellular and animal mechanistic evidence. It suggests that microplastics from plastic tableware are not ‘inert’ pollution and may directly impair sperm production through cellular autophagy and apoptosis.
The authors noted limitations, including animal doses above environmental exposure levels and the lack of actual fertility outcomes. Even so, the study provides a strong basis for understanding the relationship between microplastics and impaired male fertility.
Conclusion
The study identified a potential threat to the male reproductive system from plastic tableware use and microplastic exposure, particularly among people with low body weight or high exposure. It found that 50-nanometer PS microplastics activate the FOXA1/MAP3K1/p38 pathway, causing autophagy and apoptosis in testicular cells and impairing sperm count and motility.
The researchers called for stricter public health policies to limit microplastic release from food containers and encourage safer alternative materials.
Story source:
Collected online