article · Andrologia
Lead exposure causes significant damage to male reproductive function through distinct biochemical and molecular pathways. In an animal study, rats exposed to lead acetate in drinking water exhibited marked declines in sperm count, motility, and viability, alongside a rise in structural sperm abnormalities and degeneration within the seminiferous tubules and Leydig cells. The treatment also triggered testicular oxidative stress, evidenced by depleted antioxidant enzyme activities, specifically superoxide dismutase, glutathione peroxidase, and catalase, together with increased lipid peroxidation. In addition to altering testosterone balance, lead exposure caused a pronounced reduction in serum and testicular oestradiol levels. At the gene expression level, lead downregulated oestrogen receptor alpha and aromatase P450. These results demonstrate that lead impairs sperm production in part by generating oxidative stress and disrupting oestrogen-mediated hormonal pathways.
Lead is a common environmental pollutant known to harm reproductive health. Clarifying the precise cellular and hormonal mechanisms through which heavy metals disrupt fertility is essential for toxicologists and medical researchers. By identifying the specific enzyme pathways, oxidative markers, and oestrogen receptors affected by lead, this work helps explain how environmental toxins impair male reproductive capacity.
This is early-stage fundamental research providing biological insight into toxic mechanisms. While the identified molecular targets, such as aromatase P450 and specific antioxidant pathways, could eventually inform the screening of protective compounds by biomedical researchers, the abstract does not indicate any direct product development or commercial pathway. Practical applications remain distant from real-world use.
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This study was conducted to investigate the mechanism of lead (Pb)-induced testicular toxicity. We examined the impact of Pb toxicity on 17β-oestradiol (E2), oestrogen receptors (ERs) and aromatase P450 which are key factors in spermatogenesis. Treatment of rats with Pb acetate (PbAc, 50 mg/L in drinking water) significantly reduced sperm count, motility, viability and increased sperm abnormalities along with degenerative changes in seminiferous tubules and Leydig cells. Additionally, administration of PbAc resulted in a significant reduction in serum testosterone, serum and testicular E2 as well as increased level of testicular testosterone. Pb also induced testicular oxidative stress as evidenced by a significant decrease in the activities of superoxide dismutase, glutathione peroxidase and catalase antioxidant enzymes, and increased malondialdehyde level in the testis. At the molecular level, Pb treatment downregulated the mRNA expression of P450 arom (Cyp19) and ERα. In conclusion, Pb induces testicular oxidative damage and disrupts spermatogenesis, at least in part, via downregulation of Cyp19 and ERα expression, which further decrease E2 level. These data, therefore, provide insight into the mechanism of lead-induced testicular toxicity.
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DOI: 10.1111/and.12750
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