article · The Aging Male
Lead exposure causes significant reproductive damage in male Wistar rats, resulting in reduced body weight, decreased reproductive organ weights, and degraded sperm quality, including lower sperm count, motility, and viability alongside higher rates of abnormal morphology. Lead toxicity triggers oxidative stress by raising xanthine oxidase activity and uric acid levels while depressing key antioxidant defences. It also promotes inflammation and cell death, reduces circulating reproductive hormone levels, suppresses crucial steroidogenic enzymes, and induces severe structural degeneration in testicular tissues. Co-administering zinc successfully counteracts these damaging effects. Zinc protects the testes by lowering inflammation and oxidative stress, limiting apoptosis through the downregulation of the xanthine oxidase, uric acid, and caspase 3 pathway, and restoring essential steroid-producing enzymes. These findings demonstrate the protective role of zinc against heavy metal-induced testicular harm in an animal model.
Lead exposure remains a widespread environmental and occupational hazard that severely impairs male reproductive health and fertility. By identifying how lead induces cellular damage and hormone suppression in animal models, this research highlights the protective mechanism of zinc. Demonstrating that zinc can counteract oxidative stress and cell death offers valuable insight into potential dietary or therapeutic interventions aimed at mitigating reproductive toxicities caused by heavy metals.
This work represents early-stage animal research demonstrating the protective effect of zinc against lead-induced testicular toxicity. The findings could inform the development of protective nutritional supplements or supportive therapies for individuals in occupational settings with high heavy metal exposure. However, because the research is confined to animal models without product testing, substantial clinical validation and formulation work are required before commercial or therapeutic deployment is possible.
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AIM: This study evaluated the effect of lead, with or without zinc co-administration, on steroidogenic and xanthine oxidase (XO)/uric acid (UA)/caspase 3-mediated apoptotic signaling in the testis. MATERIALS AND METHODS: Forty male Wistar rats were divided into four groups at random; vehicle-treated control, zinc-treated, lead-treated, and lead + zinc-treated groups. RESULTS: Lead exposure significantly lowered overall weight gain, testicular, epididymal, seminal vesicle, and prostate weights. Also, lead decreased sperm count, viability and motility but increased the fraction of sperm with aberrant morphology. In addition, lead caused a marked rise in the level of UA and XO activity but a decrease in nuclear factor erythroid 2-related factor 2 (Nrf2), reduced glutathione (GSH) as well as total antioxidant capacity (TAC) levels, and superoxide dismutase (SOD) and catalase activities. Furthermore, lead increased the testicular levels of nuclear factor kappa B (NFkB), interleukin-1beta (IL-1β), and tumour necrotic factor-alpha (TNF-α), which were associated with an increase in testicular caspase 3 activity and DNA fragmentation as well as a decline in circulating gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and testicular 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-hydroxysteroid dehydrogenase (17β-HSD). These were associated with lead-induced degenerative changes in testicular tissues evidenced by shrunken seminiferous tubules, degeneration and sloughing of germ cells. Co-administration of zinc prevented lead-induced testicular injury by ameliorating oxidative stress, apoptosis, and inflammation through downregulation of XO/UA/caspase 3 pathway and upregulation of testicular 3β-HSD/17β-HSD. CONCLUSION: This study demonstrated that zinc protected against lead-induced testicular toxicity via the downregulation of XO/UA/caspase 3 signaling.
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DOI: 10.1080/13685538.2023.2224428
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