Ameliorative Effects of Vitamin C on Heat Stress-Induced Testicular Dysfunction in Wistar Rats.

IF 1.9
Damilare Rotimi, Adebanke Olaide Adesupo, Marvis Ayoola, Tomilola Debby Olaolu, Oluyomi Stephen Adeyemi
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Abstract

Objective: To evaluate the effects of repeated heat exposure on testicular function and sperm quality in Wistar rats and to determine whether vitamin C mitigates heat stress-induced reproductive damage.

Methods: Twenty-four Wistar rats were allocated to four groups and treated for 28 days: (i) control, (ii) heat exposure (40°C for 4 hours/day), (iii) vitamin C (50 mg/kg), and (iv) vitamin C plus heat exposure. Antioxidant status (superoxide dismutase, catalase, reduced glutathione), oxidative/nitrosative stress markers (malondialdehyde, nitric oxide), reproductive hormones (testosterone, follicle-stimulating hormone, luteinizing hormone), testicular function markers (alkaline phosphatase, acid phosphatase, glycogen, protein), testicular cortisol and cholesterol, histological structure, body and testis weights, and sperm parameters (concentration, total count, motility profile) were assessed.

Results: Heat exposure significantly reduced antioxidant defenses (superoxide dismutase, catalase, reduced glutathione), increased malondialdehyde and nitric oxide levels, and disrupted reproductive hormones (decreased testosterone with increased follicle-stimulating and luteinizing hormones). Heat stress also decreased alkaline and acid phosphatase activities, glycogen, and protein levels, increased testicular cortisol and cholesterol, induced histological damage, and reduced body and testis weights. Sperm quality was impaired, with lower sperm concentration, total count, and fast motility, and higher slow and non-motile sperm fractions. Vitamin C co-treatment partially attenuated these effects, improving catalase activity, Nrf-2 levels, glycogen, testosterone, alkaline and acid phosphatase, and lessened lipid peroxidation.

Conclusion: Repeated heat exposure induced oxidative stress, hormonal imbalance, impaired sperm quality, and structural testicular injury in Wistar rats. Vitamin C provided partial protection against heat-induced testicular dysfunction, supporting its potential role as an adjunct antioxidant strategy; further studies should evaluate additional antioxidants and include gene expression analyses to clarify mechanisms and fertility outcomes.

维生素C对Wistar大鼠热应激性睾丸功能障碍的改善作用。
目的:观察反复热暴露对Wistar大鼠睾丸功能和精子质量的影响,探讨维生素C是否能减轻热应激引起的生殖损伤。方法:Wistar大鼠24只,随机分为4组,每组28 d:(i)对照组,(ii)热暴露(40°C, 4 h /d), (iii)维生素C (50 mg/kg), (iv)维生素C加热暴露。评估抗氧化状态(超氧化物歧化酶、过氧化氢酶、还原性谷胱甘肽)、氧化/亚硝化应激标志物(丙二醛、一氧化氮)、生殖激素(睾酮、促卵泡激素、黄体生成素)、睾丸功能标志物(碱性磷酸酶、酸性磷酸酶、糖原、蛋白质)、睾丸皮质醇和胆固醇、组织结构、体和睾丸重量以及精子参数(浓度、总数、运动谱)。结果:热暴露显著降低抗氧化防御(超氧化物歧化酶、过氧化氢酶、还原谷胱甘肽),增加丙二醛和一氧化氮水平,破坏生殖激素(睾丸激素降低,促卵泡和促黄体激素增加)。热应激还会降低碱性和酸性磷酸酶活性、糖原和蛋白质水平,增加睾丸皮质醇和胆固醇,诱导组织学损伤,减轻体重和睾丸重量。精子质量受损,精子浓度、总数和快速运动较低,而缓慢和非运动精子比例较高。维生素C共处理部分减弱了这些影响,提高了过氧化氢酶活性、Nrf-2水平、糖原、睾酮、碱性和酸性磷酸酶,并减轻了脂质过氧化。结论:反复热暴露可引起Wistar大鼠氧化应激、激素失衡、精子质量受损和睾丸结构性损伤。维生素C对热致睾丸功能障碍提供部分保护,支持其作为辅助抗氧化策略的潜在作用;进一步的研究应评估其他抗氧化剂,并包括基因表达分析,以阐明机制和生育结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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