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Elucidating the mechanisms and mitigation strategies for six-phthalate-induced toxicity in male germ cells
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Researchers exposed male germ cells to a mixture of six phthalates and found it inhibited cell proliferation, triggered oxidative stress and apoptosis, and disrupted the PI3K/Akt/mTOR pathway, while a triple inhibitor combination successfully reversed these toxic effects, offering a potential mitigation strategy for phthalate-induced male reproductive harm.
Phthalate esters (PAEs) are primary plasticizers and endocrine-disrupting chemicals (EDCs) that are extensively used in numerous everyday consumer products. Although the adverse effects of single PAEs have been studied, our understanding of the effect of multiple phthalate exposure on male germ cell vitality remains limited. Therefore, this study aimed to investigate the collective effects of a mixture of PAEs (MP) comprising diethyl-, bis (2-ethylhexyl)-, dibutyl-, diisononyl-, diisobutyl-, and benzyl butyl-phthalates in the proportions of 35, 21, 15, 15, 8, and 5%, respectively, on differentiated male germ cells using GC-1 spermatogonia (spg) cells. As a mixture, MP substantially hindered GC-1 spg cell proliferation at 3.13 μg/mL, with a half-maximal inhibitory concentration of 16.9 μg/mL. Treatment with 25 μg/mL MP significantly induced reactive oxygen species generation and promoted apoptosis. Furthermore, MP activated autophagy and suppressed phosphorylation of phosphoinositide 3-kinase, protein kinase B, and mammalian target of rapamycin (mTOR). The triple inhibitor combination treatment comprising parthenolide, N-acetylcysteine, and 3-methyladenine effectively reversed MP-induced GC-1 spg cell proliferation inhibition, mitigated apoptosis and autophagy, and restored mTOR phosphorylation. This study is the first to elucidate the mechanism underlying MP-induced male germ cell toxicity and the restoration of male germ cell proliferation mediated by chemical inhibitors. Therefore, it provides valuable insights into the existing literature by proposing a combinatorial toxicity mitigation strategy to counteract male germ cell toxicity induced by various EDCs exposure.
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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.
Endocrine-Disrupting Chemicals and Male Infertility: Mechanisms, Risks, and Regulatory Challenges
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This review synthesizes evidence that endocrine-disrupting chemicals—including phthalates, bisphenol A, pesticides, and heavy metals—impair male fertility through oxidative stress, hormonal disruption, and epigenetic changes, while calling for improved biomonitoring, better understanding of low-dose and mixture effects, and stronger international regulation.
Quantitative analysis and toxicological mechanisms of various male infertility inducers: A network meta-analysis and pharmacological approach.
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This network meta-analysis of 201 rodent studies compared nine common male infertility inducers, finding that microplastics caused among the most severe impairments to sperm count and motility — on par with the chemotherapy drug cyclophosphamide. Oxidative stress emerged as a shared mechanistic pathway across all inducers, pointing to it as a key target for understanding and potentially mitigating reproductive harm from environmental exposures.
Simultaneous challenge with polystyrene nanoplastics and BDE-47 elicits cooperative cytotoxic impairment in human spermatozoa
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Scientists found that tiny plastic particles and a common flame retardant chemical (BDE-47), when combined, seriously damaged human sperm, even though each one alone caused little harm. Together they triggered cell stress and death in sperm, hurting their ability to swim and fertilize an egg. This suggests everyday chemical mixtures, not just single pollutants, may play a hidden role in declining male fertility.
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.
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