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阴囊温度升高,但精索静脉曲张程度没有升高,反映了睾丸氧化应激介导的细胞凋亡。

Elevated scrotal temperature, but not varicocele grade, reflects testicular oxidative stress-mediated apoptosis.

机构信息

Department of Urology, Graduate School of Medicine, Yamaguchi University, 111 Minami-Kogushi, Ube, Yamaguchi, 755-8505, Japan.

出版信息

World J Urol. 2010 Jun;28(3):359-64. doi: 10.1007/s00345-009-0462-5. Epub 2009 Aug 5.

DOI:10.1007/s00345-009-0462-5
PMID:19655149
Abstract

PURPOSE

Elevation of scrotal temperature has been known as a cause of male infertility but the exact mechanism leading to impaired spermatogenesis is unknown. This work aimed to investigate the role of elevated scrotal temperature, oxidative stress, and apoptosis in testes of infertile males associated with varicocele.

METHODS

Thirty-two testicular biopsies from patients with left varicocele who underwent preoperative measurement of scrotal temperature (DeltaT), serum follicle stimulating hormone (FSH), luteinizing hormone, and testosterone were included. Generation of 4-hydroxy-2-nonenal (4-HNE)-modified proteins and proteolytic fragments of poly(ADP-ribose) polymerase (PARP) and caspase-3 detected by Western blotting were examined as markers for oxidative stress and apoptosis, respectively. These expressions were compared with clinical parameters.

RESULTS

Irrespective of varicocele grades, sperm concentration, motility, serum FSH, and testosterone were deteriorated with the increase of DeltaT. There was a distinct correlation between generation of 4-HNE-modified proteins and DeltaT, indicating a close association between scrotal temperature and oxidative stress. Cleavages of PARP and caspase-3, which appear at 86 and 17 kDa, respectively, were strongly correlated with DeltaT and generation of 4-HNE-modified proteins.

CONCLUSIONS

Elevation of scrotal temperature is one of the major factors to impair spermatogenesis and steroidogenesis in testis with varicocele. This heat stress is shown to be closely associated with oxidative stress, following the apoptosis of germ cells.

摘要

目的

众所周知,阴囊温度升高是导致男性不育的原因之一,但导致精子发生受损的确切机制尚不清楚。本研究旨在探讨精索静脉曲张不育男性阴囊温度升高、氧化应激和细胞凋亡在睾丸中的作用。

方法

纳入 32 例因左侧精索静脉曲张而行术前阴囊温度(DeltaT)、血清卵泡刺激素(FSH)、黄体生成素和睾酮测量的患者的睾丸活检。Western 印迹法检测 4-羟基-2-壬烯醛(4-HNE)修饰蛋白和多聚(ADP-核糖)聚合酶(PARP)和半胱天冬酶-3 的蛋白水解片段的产生,分别作为氧化应激和细胞凋亡的标志物进行检测。将这些表达与临床参数进行比较。

结果

无论精索静脉曲张分级如何,精子浓度、活力、血清 FSH 和睾酮均随 DeltaT 的增加而恶化。4-HNE 修饰蛋白的产生与 DeltaT 之间存在明显的相关性,表明阴囊温度与氧化应激之间存在密切的关联。PARP 和半胱天冬酶-3 的裂解产物分别出现在 86 和 17 kDa 处,与 DeltaT 和 4-HNE 修饰蛋白的产生密切相关。

结论

阴囊温度升高是精索静脉曲张睾丸中精子发生和类固醇生成受损的主要因素之一。这种热应激与氧化应激密切相关,随后是生殖细胞凋亡。

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