Zinc improves sexual performance and erectile function by preventing penile oxidative injury and upregulating circulating testosterone in lead-exposed rats
Autor: | Elizabeth Enohnyket Besong, Tunmise Maryanne Akhigbe, Precious Jesutofunmi Ashonibare, Abimbola Ayoola Oladipo, Jacinta Nkechi Obimma, Moses Agbomhere Hamed, Damilare Hakeem Adeyemi, Roland Eghoghosoa Akhigbe |
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Jazyk: | angličtina |
Rok vydání: | 2023 |
Předmět: | |
Zdroj: | Redox Report, Vol 28, Iss 1 (2023) |
Druh dokumentu: | article |
ISSN: | 13510002 1743-2928 1351-0002 |
DOI: | 10.1080/13510002.2023.2225675 |
Popis: | ABSTRACTAim: 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. |
Databáze: | Directory of Open Access Journals |
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