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Unraveling the endocrine disruption potential of microplastics in testosterone regulation
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Researchers reviewed in vivo evidence that microplastics impair testosterone synthesis through multiple converging mechanisms — oxidative damage to Leydig cells, disruption of the LH/cAMP/StAR steroidogenesis cascade, NF-κB inflammation, and endoplasmic reticulum stress — while flagging a critical gap in human data and the largely unexplored role of physicochemical diversity among plastic types.
Microplastics (MPs) are increasingly recognized as emerging endocrine disrupting chemicals with significant implications for male reproductive health. Despite of well documentation on widespread presence in the environment, their specific effects on testosterone synthesis in humans remain insufficiently characterized. Current in vivo studies demonstrate that MPs impair androgen regulation through several interconnected mechanisms. These include oxidative stress-induced damage to Leydig cells, downregulation of antioxidant enzymes such as GPX1, disruption of the LH/cAMP/PKA/StAR signaling cascade essential for steroidogenesis, activation of NF-κB and inflammatory pathways, and induction of endoplasmic reticulum stress that accelerates testosterone metabolism. Additionally, MPs and their chemical additives interfere with steroidogenic enzymes and hormone receptors. Our review consolidates mechanistic insights linking MPs to testosterone disruption, underscores the dose-dependent nature of these effects. We also highlight critical knowledge gaps particularly the paucity of human data, the physicochemical diversity of MPs, and the long-term reversibility of endocrine disruption.
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This review consolidates evidence that microplastic exposure reduces sperm quality, disrupts spermatogenesis, and can pass toxic effects across generations in mammals, acting through inflammation, hormonal disruption, and oxidative stress. As microplastics increasingly accumulate in human reproductive organs, understanding these mechanisms is urgently important for addressing a potential contributor to declining male fertility worldwide.
Impact and mechanisms of microplastics and nanoplastics on the reproductive system
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Researchers reviewed evidence that microplastics and nanoplastics disrupt both male and female reproductive systems across multiple species, causing oxidative stress, endocrine disruption, reduced sperm quality, impaired ovarian function, and potentially transgenerational reproductive damage — with human data still limited but concerns growing.
Biochemical Effects of Microplastics on Human Health: A Comprehensive Review
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A comprehensive review documents how microplastics enter the human body through ingestion, inhalation, and skin contact, then reach the lungs, liver, kidneys, brain, and reproductive organs, triggering oxidative stress, inflammation, endocrine disruption, and genotoxicity. These biochemical pathways link microplastic exposure to serious chronic conditions including metabolic syndrome, neurodegenerative disease, reproductive dysfunction, and cancer.
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