article · Redox Report
Exposure to lead causes significant reproductive and sexual impairment in male rats, but dietary zinc supplementation counteracts these harmful effects. In an animal study where rats received oral daily treatments for twenty-eight days, lead exposure reduced mating motivation, erectile reflexes, penile weight, and sexual performance metrics. Co-administration of zinc reversed these deficits, restoring mount, intromission, and ejaculation latencies and frequencies. At the biochemical level, zinc prevented the suppression of key reproductive hormones, including testosterone, luteinising hormone, and follicle-stimulating hormone, alongside nitric oxide and dopamine. Furthermore, zinc restored essential antioxidant defences by increasing nuclear factor erythroid 2-related factor 2 signalling, glutathione, and antioxidant enzyme activities, while reducing oxidative markers such as malondialdehyde and xanthine oxidase. Overall, zinc mitigates lead-induced erectile dysfunction by curbing oxidative damage and restoring hormone balance.
Lead exposure is a persistent environmental hazard that damages male reproductive health and sexual function through oxidative tissue injury. By demonstrating that an accessible mineral supplement can reverse hormone depletion, tissue damage, and erectile difficulties in an animal model, this research highlights how targeted antioxidant therapies could potentially protect against environmental heavy metal toxicity.
This work represents early-stage, preclinical animal research that could inform the formulation of therapeutic supplements or protective dietary interventions for populations exposed to heavy metals. Potential end users include clinicians managing male infertility or occupational health specialists addressing industrial metal exposure. However, the findings are currently limited to rodent models, meaning human clinical trials and safety evaluations are necessary before any therapeutic application can be realised.
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AIM: The present study evaluated the effect of lead exposure with and without zinc therapy on male sexual and erectile function. METHODS: Twenty male Wistar rats were randomly assigned into four groups; the control, zinc-treated, lead-exposed, lead + zinc-treated groups. Administrations were per os daily for 28 days. RESULTS: Zinc co-administration significantly improved absolute and relative penile weights and the latencies and frequencies of mount, intromission, and ejaculation in lead-exposed rats. Also, zinc ameliorated lead-induced reductions in motivation to mate and penile reflex/erection. These findings were accompanied by attenuation of lead-induced suppression of circulating nitric oxide (NO), penile cyclic guanosine monophosphate (cGMP), dopamine, serum luteinizing hormone, follicle-stimulating hormone, and testosterone. In addition, zinc alleviated lead-induced upregulation of penile activities of acetylcholinesterase and xanthine oxidase (XO), and uric acid (UA) and malondialdehyde (MDA) levels. Furthermore, zinc ameliorated the lead-induced decline in penile nuclear factor erythroid 2-related factor 2 (Nrf2) and reduced glutathione (GSH) levels, and catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) activities. CONCLUSION: This study revealed that co-administration of zinc improves lead-induced sexual and erectile dysfunction by suppressing XO/UA-driven oxidative stress and upregulating testosterone via Nrf2-mediated signaling.
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DOI: 10.1080/13510002.2023.2225675
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