Zinc improves sexual and erectile function in HAART-treated rats via the upregulation of erectogenic enzymes and maintenance of redox balance

Akhigbe, R.E.; Hamed, Moses Agbomhere; Odetayo, Adeyemi Fatai; Akhigbe, T. M.; Oyedokun, P A

doi:10.1080/13685538.2023.2205517

Cited by 17 publications

(12 citation statements)

References 49 publications

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“…This study demonstrated that zinc might potentially attenuate acrylamide-induced testicular toxicity, and Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathways may be the target for the gonads-protective strategy of zinc. These results agreed with the study of Ganju and Eastman [ 44 ], Hamed et al [ 18 ], and Akhigbe et al [ 45 ], that reported that zinc suppressed oxidative stress, inflammation, and apoptosis through the modulation of pro-oxidants, antioxidants, pro-inflammatory, apoptotic and antiapoptotic proteins. The gonado-protective effect of zinc is accompanied by the restoration of testicular histoarchitecture and function by preventing degeneration of seminiferous tubules epithelium, loss of sperm cells at the lumen, degeneration of the interstitial cells and normalization of sperm qualities and reproductive hormones.…”

Section: Discussionsupporting

confidence: 92%

Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway

Ajibare,

Odetayo,

Akintoye

et al. 2024

Redox Report

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Background: Acrylamide is a toxic substance formed in some foods that require high-temperature cooking processes and has been implicated as a gonadotoxic agent. Zinc, on the other hand, is a known antioxidant with fertility-enhancing properties. Hence, this study was designed to explore the possible ameliorative effect of zinc in acrylamide-induced gonadotoxicity. Methods: Twenty-four male Wistar rats were randomized into control, acrylamide (10 mg/kg of acrylamide), acrylamide + 1 mg/kg of zinc, and acrylamide + 3 mg/kg of zinc. The administration was via the oral route and lasted for 56 days. Results: Zinc treatment ameliorated acrylamide-impaired sperm quality, normal testicular histoarchitecture, and hormonal balance, which was accompanied by increased testicular malondialdehyde and interleukin-1β and decreased testicular superoxide dismutase (SOD) and catalase (CAT). Furthermore, zinc prevented acrylamide-induced downregulation of testicular nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and B-cell lymphoma 2 (BCl2) expression and upregulation of testicular nuclear factor kappa B (NF-κB) and bcl-2-like protein 4 (bax) expression. Conclusion: In conclusion, zinc may protect against acrylamide-induced testicular toxicity, mediated by its antioxidant, anti-inflammatory, and antiapoptotic effects.

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Section: Discussionsupporting

confidence: 92%

Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway

Ajibare,

Odetayo,

Akintoye

et al. 2024

Redox Report

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“…The finding from this study that BPF decreased AChE is similar to previous studies that reported similar observations following BPF exposure 35 and its analog 36 , 37 . Although, it is expected that a decline in AChE should improve sexual function since AChE activities have been shown to breaks down or hydrolyzes acetylcholine (ACh), which is also responsible for penile erection 38 . In addition, the presence of ACh also stimulates dopamine release 39 – 41 .…”

Section: Discussionmentioning

confidence: 99%

Omega 3 fatty acid improves sexual and erectile function in BPF-treated rats by upregulating NO/cGMP signaling and steroidogenic enzymes activities

Odetayo,

Olayaki

2023

Sci Rep

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Bisphenol F (BPF) is an environmental pollutant that has been implicated in sexual dysfunction. Omega 3 fatty acid (O3FA), on the other hand, is an antioxidant with the ability to improve fertility indices. However, no study has explored the possible ameliorative effect of O3FA on BPF-induced sexual dysfunction. Thus, the effect of BPF and/or O3FA on male sexual performance was investigated. Male Wistar rats were randomized into 6 groups, corn oil-treated, O3FA low and high dose (100 and 300 mg/kg), BPF-treated, BPF + O3FA low and BPF + O3FA high dose. BPF significantly impaired male sexual competence, evidenced by a reduction in motivation to mate, prolonged mount, intromission and ejaculation latency, and post-ejaculatory index. Furthermore, a reduction in mount, intromission, and ejaculation frequency were observed. Also, BPF caused a decrease in gonadotropin releasing hormone, follicle stimulating hormone, luteinizing hormone, testosterone, nitric oxide (NO) cyclic guanosine monophosphate (cGMP), 3beta-hydroxysteroid dehydrogenase (3β-HSD), 17beta-hydroxysteroid dehydrogenase (17β-HSD), dopamine, and acetylcholine esterase. Furthermore, it was accompanied by a significant increase in prolactin and estrogen and poor pregnancy outcomes. These observed BPF-led alterations were abolished by O3FA administration. This study showed that O3FA ameliorates BPF-induced sexual dysfunction by upregulating NO/cGMP signaling and steroidogenic enzymes activities.

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“…Testosterone is required for maintaining spermatogenesis, and the production of mature sperm is intimately dependent on androgen action within the testis. In fact, the maintenance of optimal sexual and erectile function depends on the effective testosterone secretion ( 78 , 79 ). Testosterone is also responsible for different biological processes and is important for the development and maintenance of male secondary characteristics.…”

Section: Gnihmentioning

confidence: 99%

Impact of stress on male fertility: role of gonadotropin inhibitory hormone

Odetayo,

Akhigbe,

Bassey

et al. 2024

Front. Endocrinol.

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Studies have implicated oxidative stress-sensitive signaling in the pathogenesis of stress-induced male infertility. However, apart from oxidative stress, gonadotropin inhibitory hormone (GnIH) plays a major role. The present study provides a detailed review of the role of GnIH in stress-induced male infertility. Available evidence-based data revealed that GnIH enhances the release of corticosteroids by activating the hypothalamic-pituitary-adrenal axis. GnIH also mediates the inhibition of the conversion of thyroxine (T4) to triiodothyronine (T3) by suppressing the hypothalamic-pituitary-thyroidal axis. In addition, GnIH inhibits gonadotropin-releasing hormone (GnRH), thus suppressing the hypothalamic-pituitary-testicular axis, and by extension testosterone biosynthesis. More so, GnIH inhibits kisspeptin release. These events distort testicular histoarchitecture, impair testicular and adrenal steroidogenesis, lower spermatogenesis, and deteriorate sperm quality and function. In conclusion, GnIH, via multiple mechanisms, plays a key role in stress-induced male infertility. Suppression of GnIH under stressful conditions may thus be a beneficial prophylactic and/or therapeutic strategy.

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Zinc improves sexual and erectile function in HAART-treated rats via the upregulation of erectogenic enzymes and maintenance of redox balance

Cited by 17 publications

References 49 publications

Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway

Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway

Omega 3 fatty acid improves sexual and erectile function in BPF-treated rats by upregulating NO/cGMP signaling and steroidogenic enzymes activities

Impact of stress on male fertility: role of gonadotropin inhibitory hormone

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