Alahwany Ahmed Mohamed, Arisha Ahmed Hamed, Abdelkhalek Adel, Khamis Tarek, Miyasho Taku, Kirat Doaa
Department of Animal Physiology and Biochemistry, Faculty of Veterinary Medicine, Badr University in Cairo (BUC), Badr City 11829, Egypt.
Department of Physiology, Faculty of Veterinary Medicine, Zagazig University, Zagazig 44519, Egypt.
Int J Mol Sci. 2025 Jan 1;26(1):316. doi: 10.3390/ijms26010316.
While ultraviolet C (UVC) radiation has beneficial applications, it can also pose risks to living organisms. Nevertheless, a detailed assessment of UVC radiation's effects on mammalian male reproductive physiology, including the underlying mechanisms and potential protective strategies, has not yet been accomplished. This study aimed to examine the critical roles of oxidative stress, autophagy, reproductive hormonal axis, and microRNAs in UVC-induced reproductive challenges in male rats. Semen, biochemical, molecular, and in silico analyses revealed significant dysregulation of testicular steroidogenesis, impaired spermatogenesis, deteriorated sperm quality, and altered reproductive hormonal profiles, which ultimately lead to a decline in fertility in male rats exposed to UVC radiation. Our data indicated that the suppression of autophagy, stimulation of gonadotropin-inhibiting hormone (GnIH), and alteration of microRNAs serve as key mediators of UVC-induced stress effects in mammalian reproduction, potentially contributing to male infertility. Targeting these pathways, particularly through pretreatment with hesperidin (HES), offers a promising strategy to counteract UVC-induced male infertility. In conclusion, the present findings emphasize the importance of understanding the molecular mechanisms behind UVC-induced male infertility and offer valuable insights into the protective mechanisms and prospective role of HES in safeguarding male reproductive health.
虽然紫外线C（UVC）辐射有有益的应用，但它也会对生物有机体构成风险。然而，尚未完成对UVC辐射对哺乳动物雄性生殖生理学影响的详细评估，包括其潜在机制和潜在的保护策略。本研究旨在探讨氧化应激、自噬、生殖激素轴和微小RNA在UVC诱导的雄性大鼠生殖挑战中的关键作用。精液、生化、分子和计算机分析显示，睾丸类固醇生成显著失调、精子发生受损、精子质量恶化以及生殖激素谱改变，这最终导致暴露于UVC辐射的雄性大鼠生育能力下降。我们的数据表明，自噬的抑制、促性腺激素抑制激素（GnIH）的刺激以及微小RNA的改变是UVC诱导的哺乳动物生殖应激效应的关键介质，可能导致雄性不育。针对这些途径，特别是通过橙皮苷（HES）预处理，提供了一种对抗UVC诱导的雄性不育的有前景的策略。总之，本研究结果强调了理解UVC诱导雄性不育背后分子机制的重要性，并为HES在保护雄性生殖健康方面的保护机制和潜在作用提供了有价值的见解。
