Hydrogen sulfide alleviates acrylamide-induced testicular toxicity in male rats.

Autor: Mokhlis, Hamada Ahmed, Rashed, Mohammed Helmy, Saleh, Ibrahim Ghalib, Eldeib, Mahmoud Gomaa, El-Husseiny, Ahmed A., Khidr, Emad Gamil, Gomaa, Maher H., Gad, Hesham S., Aglan, Ahmed
Zdroj: Toxicology & Environmental Health Sciences; Mar2023, Vol. 15 Issue 1, p41-51, 11p
Abstrakt: Objective: Testicular tissues and sperms are typically vulnerable to oxidative stress and inflammation. Despite functioning as a signaling molecule in different physiological and pathological processes, hydrogen sulfide (H2S) role in the reproductive system is not fully recognized. This study aimed to assess whether H2S could counteract the testicular damage that acrylamide (AC) causes in male rats. Methods: Forty male rats were equally divided randomly into four groups: normal control, AC, H2S, and AC + H2S who received normal saline, 40 mg/Kg of AC, 200 µg/Kg of sodium hydrosulfide NaHS (H2S donor), and 40 mg/Kg of AC + 200 µg/Kg of NaHS by intraperitoneal injection for 14 consecutive days, respectively. Body and testes weights, sperm count and motility, lactate dehydrogenase isoenzyme-x (LDH-X), serum testosterone level, oxidative parameters, the expression level of inducible nitric oxide synthase (iNOS), inflammatory cytokines, and histopathological alterations were evaluated. Results: The reduction in relative testicular weights, sperm count, and motility served as evidence of the harmful effects of AC. However, these values were reversed when H2S and AC were combined. Additionally, AC significantly decreased serum testosterone level, testicular LDH-X activity, superoxide dismutase, catalase, and reduced glutathione. While malondialdehyde, expression levels of iNOS protein and inflammatory cytokines (TNF-α, IL-1β, and IL-6) levels were elevated. Interestingly, the co-administration of H2S with AC reversed these values, demonstrating an opposing effect in the previous parameters. Conclusion: H2S exhibited a protective effect in the rat model of testicular toxicity induced by AC, which may be associated with the suppression of iNOS expression, proinflammatory cytokines, and the inhibition of oxidative stress injury. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index