Long term testicular ischemia-reperfusion injury-induced apoptosis: Involvement of survivin down-regulation

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dc.contributor.author Al-Maghrebi, M.
dc.contributor.author Kehinde, E.O.
dc.contributor.author Anim, J.T.
dc.date.accessioned 2013-06-21T17:46:36Z
dc.date.accessioned 2017-10-19T12:43:53Z
dc.date.available 2013-06-21T17:46:36Z
dc.date.available 2017-10-19T12:43:53Z
dc.date.issued 2010-05-07
dc.identifier.citation Al-Maghrebi, M., Kehinde, E. O., & Anim, J. T. (2010). Long term testicular ischemia-reperfusion injury-induced apoptosis: Involvement of survivin down-regulation. Biochemical and Biophysical Research Communications, 395(3), 342-347. Link to full text: http://hinari-gw.who.int/whalecomwww.sciencedirect.com/whalecom0/science/article/pii/S0006291X10006741 en_US
dc.identifier.issn 0006291X
dc.identifier.uri http://197.255.68.203/handle/123456789/3913
dc.description.abstract Testicular torsion is associated with damage to the testicular tissue as a result of ischemia-reperfusion injury (IRI) and induction of apoptosis leading to progressive damage to spermatogenesis. Survivin is suggested to be an important regulator in the control of the mitochondrial apoptotic pathway, although its role in torsion-induced IRI is unknown. Therefore, we sought to evaluate testicular survivin expression after long term IRI induced by testicular torsion. Survivin expression was measured by real-time PCR in 6-12 month old New Zealand white rabbits divided into three groups (4 animals/group): group (A) sham control, group (B) ischemia alone for 60 min and group (C) ischemia for 60 min followed by reperfusion for 6 months. Germ cell apoptosis was evaluated by TUNEL assay, Bax/Bcl-2 ratio and DNA fragmentation. The Johnsen score was used to assess testicular morphological damage, while lipid peroxidation was used as an indicator for oxidative stress. Survivin expression was detected in all testicular tissue samples. The rate of survivin expression after IRI was significantly higher (p < 0.05) compared with ischemic only and sham control testes. Its expression in IRI samples was inversely correlated with the significant increase (p < 0.05) in apoptosis, oxidative levels and spermatogenic damage. In conclusion, down-regulation of testicular survivin expression after long term IRI to the testis and its association with apoptosis induction suggests its involvement in the regulation of this apoptotic pathway. These findings also identify survivin as a potential new target for the prevention of germ cell death during testicular torsion. en_US
dc.language.iso en en_US
dc.publisher Biochemical and Biophysical Research Communications en_US
dc.subject Apoptosis en_US
dc.subject Ischemia-reperfusion injury en_US
dc.subject Survivin en_US
dc.subject Testicular torsion en_US
dc.title Long term testicular ischemia-reperfusion injury-induced apoptosis: Involvement of survivin down-regulation en_US
dc.type Article en_US


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