Graduate School of Biomedical Sciences, Tokushima University, 1-78-1 Shomachi, Tokushima, 770-8505, Japan; Department of Biochemistry, Faculty of Veterinary Medicine, Zagazig University, El-Shohada, Moawwad, Qesm Awel AZ, Zagazig, 44511, Egypt.
Graduate School of Biomedical Sciences, Tokushima University, 1-78-1 Shomachi, Tokushima, 770-8505, Japan.
J Therm Biol. 2023 Feb;112:103465. doi: 10.1016/j.jtherbio.2023.103465. Epub 2023 Jan 9.
Heat is a detrimental environmental stressor that disrupts spermatogenesis and results in male infertility. Previous investigations have shown that heat stress reduces the motility, number, and fertilization ability of living spermatozoa. Sperm hyperactivation, capacitation, acrosomal reaction, and chemotaxis towards the ova are regulated by the cation channel of sperm (CatSper). This sperm-specific ion channel triggers the influx of calcium ions into sperm cells. The aim of this study in rats was to investigate whether heat treatment affected the expression levels of CatSper-1 and -2, together with the sperm parameters, testicular histology and weight. The rats were exposed to heat stress for 6 days and the cauda epididymis and testis were collected 1, 14, and 35 days after heat treatment to measure sperm parameters, gene and protein expression, testicular weight, and histology. Interestingly, we found that heat treatment caused a notable downregulation of CatSper-1 and -2 expression at all three time points. In addition, there were significant reductions in sperm motility and number and an increase in the percentage of abnormal sperm at 1 and 14 days, with cessation of sperm production at 35 days. Furthermore, expression of the steroidogenesis regulator, 3 beta-hydroxysteroid dehydrogenase (3β-HSD) was upregulated in the 1-, 14- and 35-day samples. Heat treatment also upregulated the expression of the apoptosis regulator, BCL2-associated X protein (BAX), decreased testicular weight, and altered testicular histology. Therefore, our data showed for the first time that heat stress downregulated CatSper-1 and -2 in the rat testis, and that this may be a mechanism involved in heat stress-induced impairment of spermatogenesis.
热是一种有害的环境应激源，会破坏精子发生，导致男性不育。先前的研究表明，热应激会降低活精子的活力、数量和受精能力。精子超激活、获能、顶体反应和向卵子的趋化性受精子阳离子通道（CatSper）调节。这种精子特异性离子通道触发钙离子流入精子细胞。本研究旨在探讨热应激是否会影响 CatSper-1 和 -2 的表达水平以及精子参数、睾丸组织学和重量。大鼠暴露于热应激 6 天，在热应激后 1、14 和 35 天收集附睾尾和睾丸，以测量精子参数、基因和蛋白质表达、睾丸重量和组织学。有趣的是，我们发现热应激在所有三个时间点都导致 CatSper-1 和 -2 的表达明显下调。此外，在 1 天和 14 天，精子活力和数量显著减少，畸形精子比例增加，在 35 天停止精子生成。此外，类固醇生成调节剂 3β-羟类固醇脱氢酶（3β-HSD）的表达在 1 天、14 天和 35 天的样本中上调。热应激还上调了凋亡调节剂 B 细胞淋巴瘤-2 相关 X 蛋白（BAX）的表达，降低了睾丸重量并改变了睾丸组织学。因此，我们的数据首次表明，热应激下调了大鼠睾丸中的 CatSper-1 和 -2，这可能是热应激引起精子发生损伤的机制之一。
