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Unraveling the endocrine disruption potential of microplastics in testosterone regulation
Summary
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.