THE MOLECULAR PATHOLOGY OF EXPERIMENTAL TESTICULAR TORSION SUGGESTS ADJUNCT THERAPY TO SURGICAL REPAIR

睾丸扭转 医学 生殖细胞 支持细胞 精子发生 细胞凋亡 睾丸萎缩 间质细胞 睾丸 男科 病理 内科学 外科 激素 生物 促黄体激素 基因 生物化学
作者
Terry T. Turner,Hyun J. Bang,JEFFERY L. LYSIAK
出处
期刊:The Journal of Urology [Lippincott Williams & Wilkins]
卷期号:172 (6 Part 2): 2574-2578 被引量:141
标识
DOI:10.1097/01.ju.0000144203.30718.19
摘要

No AccessJournal of UrologyOriginal Articles1 Dec 2004THE MOLECULAR PATHOLOGY OF EXPERIMENTAL TESTICULAR TORSION SUGGESTS ADJUNCT THERAPY TO SURGICAL REPAIR TERRY T. TURNER, HYUN J. BANG, and JEFFERY L. LYSIAK TERRY T. TURNERTERRY T. TURNER More articles by this author , HYUN J. BANGHYUN J. BANG More articles by this author , and JEFFERY L. LYSIAKJEFFERY L. LYSIAK More articles by this author View All Author Informationhttps://doi.org/10.1097/01.ju.0000144203.30718.19AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: We review the work of our laboratory in discovering the pathophysiological mechanisms that underpin testicular response to testicular torsion. Evidence from animal models is used to discover pathways that might be amenable to manipulation by therapeutic regimens. Materials and Methods: Rats and mice were subjected to 1 and 2 hours of testicular torsion, respectively. Preliminary experiments determined that those are the times of torsion in those species that produce severe testicular atrophy and germ cell apoptosis. A variety of biochemical and molecular biological techniques were used to determine the mechanism(s) leading to spermatogenic disruption and germ cell apoptosis. Results: Testicular torsion can eliminate spermatogenesis despite return blood flow, continued Sertoli cell function and perhaps the continued production of testosterone by Leydig cells, although the latter point is not completely resolved. Torsion repair is followed by a period of germ cell apoptosis, accumulation of testicular neutrophils and increased testicular oxidative stress. Testicular vascular E-selectin expression is increased after torsion repair as are a number of cytokines important to the recruitment of neutrophils. Elements of the c-Jun-N-terminal kinase pathway are important in this process. The presence of neutrophils leads to intratesticular oxidative stress, and oxidative stress has been significantly reduced by intravenous infusion of oxygen radical scavengers at the time of torsion repair. Conclusions: Testicular torsion causes loss of spermatogenesis and a significant increase in germ cell apoptosis due to an increase in testicular oxidative stress concomitant with reperfusion. Oxidative stress arises with recruitment of neutrophils, and the recruitment of neutrophils occurs due to E-selectin expression on the surface of the testicular venules after torsion repair. The cytokines, tumor necrosis factor-α and interleukin-1β, activate the stress related kinase pathway to E-selectin expression after torsion repair. Oxidative stress is relieved by infusion of oxygen radical scavengers, which results in a significant salvage of testicular function. References 1 : Acute scrotal pain. Emerg Med Clin North Am1998; 16: 781. 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Google Scholar From the Departments of Urology and Cell Biology, University of Virginia School of Medicine, Charlottesville, Virginia© 2004 by American Urological Association, Inc.FiguresReferencesRelatedDetailsCited byWatson M, Bartkowski D and Nelson N (2014) Intracompartmental Pressure as a Predictor of Intratesticular Blood Flow: A Rat ModelJournal of Urology, VOL. 193, NO. 6, (2062-2067), Online publication date: 1-Jun-2015.Jiang D, Wu D, Zhang Y, Xu B, Sun X and Li Z (2012) Protective Effects of Hydrogen Rich Saline Solution on Experimental Testicular Ischemia-Reperfusion Injury in RatsJournal of Urology, VOL. 187, NO. 6, (2249-2253), Online publication date: 1-Jun-2012.Yang S, Shih H, Chow Y, Wang T, Tsai P and Huang C (2010) Simvastatin Attenuates Testicular Injury Induced by Torsion-DetorsionJournal of Urology, VOL. 184, NO. 2, (750-756), Online publication date: 1-Aug-2010.Yang S, Shih H, Chow Y, Tsai P and Huang C (2008) Hemin Induced Heme Oxygenase-1 Over Expression Involves Nuclear Factor-E2 Related Factor-2, Nuclear Factor-κB and Extracellular Regulated Kinase: An Experimental Study in a Testicular Torsion-Detorsion Rodent ModelJournal of Urology, VOL. 179, NO. 6, (2456-2463), Online publication date: 1-Jun-2008. (2007) Reply by AuthorsJournal of Urology, VOL. 178, NO. 3, (1017-1017), Online publication date: 1-Sep-2007.Yang S, Shih H, Chow Y, Tsai P, Wang T, Wang P and Huang C (2018) The Protective Role of Heme Oxygenase-1 Induction on Testicular Tissues After Testicular Torsion and DetorsionJournal of Urology, VOL. 177, NO. 5, (1928-1933), Online publication date: 1-May-2007. Volume 172Issue 6 Part 2December 2004Page: 2574-2578 Advertisement Copyright & Permissions© 2004 by American Urological Association, Inc.Keywordsoxidative stresstesticular torsiontestisspermatogenesisapoptosisMetricsAuthor Information TERRY T. TURNER More articles by this author HYUN J. BANG More articles by this author JEFFERY L. LYSIAK More articles by this author Expand All Advertisement PDF downloadLoading ...
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