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Prenatal DEHP exposure induces lifelong testicular toxicity by continuously interfering with steroidogenic gene expression
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Researchers found that prenatal exposure to DEHP, a common plasticizer, causes lasting testicular toxicity in males by persistently disrupting the expression of genes involved in steroid hormone production, suggesting a mechanistic link between early-life phthalate exposure and adult male reproductive disorders including potential accelerated reproductive aging.
Prenatal DEHP exposure induces lifelong testicular toxicity by continuously interfering with steroidogenic gene expression, thus indicating the association between prenatal exposure and DSD, adult male disorders, and reproductive aging.
More Papers Like This
Prenatal DEHP exposure induces lifelong testicular toxicity by continuously interfering with steroidogenic gene expression
AI summary Read the abstract
This animal study found that exposure to DEHP — a plasticizer found in many PVC plastic products — before birth caused lasting damage to male reproductive health across the entire lifespan, from genital development problems in infancy through poor sperm quality and premature reproductive aging in adulthood. The mechanism appears to be lifelong disruption of the genes that control testosterone production, raising concerns about human health risks from early-life plastic chemical exposure.
Reproductive Toxicity of Chronic Exposure To Polystyrene Microplastics And The Molecular Mechanism of Decrease In Testosterone Levels In Male Mice
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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.
The emerging risk of exposure to nano(micro)plastics on endocrine disturbance and reproductive toxicity: From a hypothetical scenario to a global public health challenge
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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.
Prenatal microplastic exposure-induced testicular developmental toxicity and its long-term hazards in male rat offspring.
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Pregnant rats were given microplastics during pregnancy, and their male offspring had lower birth weights, smaller testicles, reduced testosterone and luteinizing hormone levels, fewer hormone-producing Leydig cells, and changes in sperm, effects that persisted from birth into adulthood.
Fetal exposure to endocrine disrupting-bisphenol A (BPA) alters testicular fatty acid metabolism in the adult offspring: relevance to sperm maturation and quality
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This study showed that prenatal exposure to bisphenol A in rats altered testicular fatty acid metabolism in adult male offspring, reducing levels of polyunsaturated fatty acids essential for sperm quality and function, linking early BPA exposure to lasting male reproductive effects.
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