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Article Tier 2 Human Health Effects Reproductive & Development Sign in to save

Faculty Opinions recommendation of Chronic exposure to polystyrene microplastics induced male reproductive toxicity and decreased testosterone levels via the LH-mediated LHR/cAMP/PKA/StAR pathway.

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Polymers
Body Systems

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Chronic exposure to polystyrene microplastics induced male reproductive toxicity and decreased testosterone levels via the LH-mediated LHR/cAMP/PKA/StAR pathway

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Mice exposed to polystyrene microplastics in their drinking water for 180 days showed significant reproductive damage, including reduced testosterone, lower sperm quality, and changes in testicular structure. The researchers identified a specific hormonal pathway through which microplastics suppress testosterone production in the cells that make it. This long-term, low-dose study is particularly relevant because the exposure levels are closer to what humans might experience in everyday life.

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Chronic exposure to polystyrene microplastics lowered testosterone levels in male mice and disrupted reproductive organ function. The study identified molecular pathways through which microplastics interfere with male hormone production, with implications for reproductive health in humans exposed through diet.

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Researchers administered polystyrene nanoplastics orally to male rats for five weeks and found significant reductions in testosterone, LH, and FSH levels, sperm DNA damage, altered testicular gene expression, and dose-dependent histological lesions, indicating that nanoplastic exposure disrupts the hormonal axis governing male reproductive function.

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Chronic exposure to polystyrene microplastics induced LHR reduction and decreased testosterone levels through NF-κB pathway

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Mice given drinking water containing polystyrene microplastics for 180 days showed significant drops in testosterone levels through a newly identified mechanism. The microplastics triggered immune cells in the testes to release inflammatory signals that suppressed a key hormone receptor (LHR), disrupting the entire hormonal pathway needed for testosterone production. This finding adds to growing evidence that microplastic exposure may impair male reproductive health.

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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.

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