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Enhanced reproductive toxicities induced by phthalates contaminated microplastics in male mice (Mus musculus)
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Researchers investigated the combined reproductive toxicity of phthalate-contaminated microplastics in male mice over a 30-day exposure period. They found that microplastics enhanced the accumulation of phthalates in the liver and gut, and the combination significantly worsened reproductive damage including reduced sperm quality and testicular tissue changes. The study suggests that microplastics may amplify the harmful effects of chemical contaminants they carry by increasing their bioavailability in the body.
It has been demonstrated that microplastics (MPs) can transport phthalate esters (PAEs) into the tissues of mice. However, the influence of MPs on accumulation of PAEs and the combined toxicity need profound investigation. In this study, the bioaccumulation of PAEs and reproductive toxicity due to contaminated MPs exposure were investigated. After exposure to PAE-contaminated MPs for 30 days, significantly increased accumulation of PAE was observed in the liver and gut but not in the testis, which are ascribed to the distribution of MPs in tissues. Herein, most micro-size MPs accumulated in the gut and liver, while only a few nano-size MPs entered the Sertoli cells. Compared with virgin MPs and PAEs alone, PAE-contaminated MPs induced enhanced reproductive toxicities manifested by greater alterations in sperm physiology and spermatogenesis. The enhanced toxicities were also confirmed by the testicular transcriptomic alterations and aggravated oxidative stress induced by PAE-contaminated MPs. These aggravated reproductive toxicities were not caused solely by PAE, but may also be caused by the sensitization effect of oxidative stress induced by MPs. Our results highlight the potential reproductive toxicity on male terrestrial mammals due to co-exposure of MPs and plastic additives and provide valuable insights into the mechanism of combined toxicity of MPs and other pollutants.
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The single and combined effects of decabromodiphenyl ethane and mixed microplastics on male mice reproductive toxicity
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Researchers investigated the combined reproductive toxicity of mixed microplastics and the flame retardant DBDPE in male mice over seven weeks. The study found that DBDPE alone decreased sex hormone levels and sperm count, and when combined with microplastics, the effects on testicular damage, sperm malformation, and oxidative stress were compounded, suggesting that microplastics may amplify the toxicity of co-occurring chemical contaminants.
Co-exposure to polystyrene microplastics and microcystin-LR aggravated male reproductive toxicity in mice
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Researchers found that exposing mice to a combination of polystyrene microplastics and microcystin-LR, a toxin produced by algae, caused more severe damage to male reproductive organs than either pollutant alone. The microplastics increased the amount of the toxin that accumulated in testicular tissue. The study suggests that the interaction between microplastics and other environmental contaminants may amplify reproductive health risks.
Lactating exposure to microplastics at the dose of infants ingested during artificial feeding induced reproductive toxicity in female mice and their offspring
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When nursing mice were exposed to microplastics at levels matching what infants ingest from plastic baby bottles, the mothers developed reproductive problems including delayed puberty, irregular cycles, and reduced fertility. Strikingly, their male offspring also showed decreased sperm count and quality, even though they were only exposed through breast milk. This suggests microplastics can cause reproductive harm that passes from mother to child, with males being especially vulnerable.
Polystyrene nanoparticles enhance the adverse effects of di-(2-ethylhexyl) phthalate on male reproductive system in mice
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Researchers investigated the combined reproductive toxicity of polystyrene nanoparticles and the plasticizer DEHP in male mice over 35 days. The study found that co-exposure to nanoparticles and DEHP produced enhanced adverse effects on sperm quality and testicular tissue compared to either substance alone, suggesting nanoplastics may amplify the endocrine-disrupting effects of plasticizers.
Synergistic assault of DEHP and MPs: Unmasking the ER stress-triggered autophagic injury male fertility
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Researchers found that mice co-exposed to microplastics and the common plasticizer DEHP through drinking water experienced severe impairment of male reproductive function, including disrupted testicular structure, declining sperm quality, and hormonal dysregulation. The combined exposure activated endoplasmic reticulum stress and triggered excessive autophagy, contributing to reproductive damage beyond what either pollutant caused alone. The study highlights the significant risks of simultaneous exposure to microplastics and plastic additives for male fertility.
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