Testicular hypofunction caused by activating p53 expression induced by reactive oxygen species in varicocele rats. (22nd January 2015)

• Record Type: Journal Article
• Authors: Liang, M.; Wen, J.; Dong, Q.; Zhao, L.‐G.; Shi, B.‐K.
• Is Part Of: Andrologia. Volume 47:Number 10(2015)
• Page Start: 1175
• Page End: 1182
• Publication Date: 2015-01-22
• Subjects: Hypoxia‐inducible factor‐1 alpha subunit -- reactive oxygen species -- testicular hypofunction -- tumour suppressor protein p53 -- varicocele; Andrology -- Periodicals; Infertility, Male -- Periodicals; 616.69
• DOI: 10.1111/and.12400
• Languages: English
• ISSNs: 0303-4569

Abstract

Summary: We investigated the mechanism of the testicular hypofunction induced by hypoxia in varicocele rats. Varicocele was induced by partial ligation of the left renal vein. Seven weeks later, left testis mass index was measured. The sperm counts and motility were tested by CASA. The change of seminiferous tubule tissue was observed by HE staining. The reactive oxygen species (ROS) level in left testicular tissue was measured by ELISA, and the expressions of HIF‐1α and p53 were detected by immunohistochemistry and Western blot. The left testis mass index and the sperm motility were significantly lower in surgery group. By HE staining, the left seminiferous epithelial cell arrangement was incompact, disordered and vacuolated in surgery group. The ROS level in surgery group was significantly higher than the other groups. The results of immunohistochemistry and Western blot indicated that the expressions of HIF‐1α and p53 increased significantly in surgery group. Our study demonstrated that varicocele caused hypoxia that could cause the rise of ROS level to induce the increase of p53 expression, leading to the decrease of testis mass index and changes of seminiferous tubules, which would reduce sperm motility and result in male infertility eventually.