The role of reactive oxygen species and apoptosis in the pathogenesis of varicocele in a rat model and efficiency of vitamin E treatment

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dc.contributor.authorÇam, Kamil
dc.contributor.authorŞimşek, Ferruh
dc.contributor.authorYüksel, Meral
dc.contributor.authorTürkeri, Levent
dc.contributor.authorHaklar, Goncagül
dc.contributor.authorYalçın, Süha
dc.contributor.authorAkdaş, Atıf Mahmut
dc.date.accessioned2020-04-30T23:34:30Z
dc.date.available2020-04-30T23:34:30Z
dc.date.issued2004
dc.departmentDÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.descriptionYuksel, Meral/0000-0002-4760-3306;en_US
dc.descriptionWOS: 000223203000006en_US
dc.descriptionPubMed: 15271202en_US
dc.description.abstractWe investigated role of reactive oxygen species (ROS) and apoptosis in the pathogenesis of infertility in experimental model of varicocele. The protective effect of vitamin E was also examined. Three groups of rats were constructed as the first group had sham operation, experimental varicoceles were established by partial ligation of the left renal vein in later two groups. Third group had received vitamin E. Production of ROS was determined by chemiluminescence assay (CL). The in situ end labelling technique was utilized to investigate apoptosis. Tissue vitamin E levels were measured by high performance liquid chromatography. The differences between luminol enhanced CL levels of groups were not statistically significant. However, the difference between CL levels of lucigenin probe in left testicles of sham and varicocele groups were statistically significant (p = 0.0007). Similarly, the results of the third group receiving vitamin E significantly differed from the varicocele group (p = 0.0025). The difference of apoptotic index was also statistically significant between sham and varicocele groups (p = 0.0038). Although the values of apoptotic index detected in the vitamin E group were lower compared with the varicocele group, the difference was not significant. This study proposes that ROS production and apoptosis in the testicles were induced with experimental varicocele. Vitamin E had a protective role. An increased rate of apoptosis with experimental varicocele suggests a molecular alteration, which may involve ROS overproduction as the triggering mechanism. Consequently, this study indicates an association between varicocele and infertility at molecular level through stimulation of ROS and apoptosis.en_US
dc.identifier.doi10.1111/j.1365-2605.2004.00476.xen_US
dc.identifier.endpage233en_US
dc.identifier.issn0105-6263
dc.identifier.issue4en_US
dc.identifier.startpage228en_US
dc.identifier.urihttps://doi.org/10.1111/j.1365-2605.2004.00476.x
dc.identifier.urihttps://hdl.handle.net/20.500.12684/5174
dc.identifier.volume27en_US
dc.identifier.wosWOS:000223203000006en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherBlackwell Publishing Ltden_US
dc.relation.ispartofInternational Journal Of Andrologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectapoptosisen_US
dc.subjectpathophysiologyen_US
dc.subjectreactive oxygen speciesen_US
dc.subjectvaricoceleen_US
dc.titleThe role of reactive oxygen species and apoptosis in the pathogenesis of varicocele in a rat model and efficiency of vitamin E treatmenten_US
dc.typeArticleen_US

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