Effect of sunitinib on testicular oxidative and proinflammatory damage induced by ischemia–reperfusion in rats; [Efecto de sunitinib en el daño oxidativo y proinflamatorio testicular inducido por isquemia-reperfusión en ratas]

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Introduction: This study aimed to biochemically and histopathologically investigate the effect of sunitinib on oxidative testicular damage induced by ischemia/reperfusion in rats. Material-method: Experimental animals were divided into three groups of six rats each: testicular torsion–detorsion (TTD), sunitinib + testicular torsion–detorsion (STD), and sham control (SC). Sunitinib (25 mg/kg) was administered orally to the STD group by gavage. Normal saline (0.9% NaCl) was administered orally to the TTD and control groups as the solvent. One hour after administration of sunitinib and 0.9% NaCl, all animal groups were done torsion–detorsion. Then, all the rats were killed by high-dose anesthesia, and their testicles were removed. Biochemical and histopathological examinations were performed on the removed testicular tissues. Results: Malondialdehyde; it was observed that the results in the STD group were close to those of the SC group and statistically significant lower compared to the TTD group (p = 0.001). The glutathione values were statistically significantly higher in the STD group compared to the TTD group (p < 0.001). Nuclear factor kappa B values, revealing a statistically significant difference between the TTD and STD groups (p < 0.001). The TNF-α levels were measured and indicating that the results of the STD group were statistically significantly lower than those of the TTD group (p < 0.001). Histopathologically, animal tissues given sunitinib were observed to resemble normal tissues. Conclusion: Sunitinib was shown to prevent histopathological changes in testicular tissue against ischemia/reperfusion damage. © 2021 Asociación Española de Andrología, Medicina Sexual y Reproductiva

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AlanDeğerDil
dc.contributor.authorKeskin, Ercument
dc.contributor.authorErdogan, Abdullah
dc.contributor.authorSuleyman, Halis
dc.contributor.authorYazici, Gulce Naz
dc.contributor.authorSunar, Mukadder
dc.contributor.authorGul, Mehmet Ali
dc.date.accessioned2026-10-18T20:27:36.388415027Z
dc.date.available2026-10-18T20:27:36.388415027Z
dc.date.issued2022
dc.description.abstractIntroduction: This study aimed to biochemically and histopathologically investigate the effect of sunitinib on oxidative testicular damage induced by ischemia/reperfusion in rats. Material-method: Experimental animals were divided into three groups of six rats each: testicular torsion–detorsion (TTD), sunitinib + testicular torsion–detorsion (STD), and sham control (SC). Sunitinib (25 mg/kg) was administered orally to the STD group by gavage. Normal saline (0.9% NaCl) was administered orally to the TTD and control groups as the solvent. One hour after administration of sunitinib and 0.9% NaCl, all animal groups were done torsion–detorsion. Then, all the rats were killed by high-dose anesthesia, and their testicles were removed. Biochemical and histopathological examinations were performed on the removed testicular tissues. Results: Malondialdehyde; it was observed that the results in the STD group were close to those of the SC group and statistically significant lower compared to the TTD group (p = 0.001). The glutathione values were statistically significantly higher in the STD group compared to the TTD group (p < 0.001). Nuclear factor kappa B values, revealing a statistically significant difference between the TTD and STD groups (p < 0.001). The TNF-α levels were measured and indicating that the results of the STD group were statistically significantly lower than those of the TTD group (p < 0.001). Histopathologically, animal tissues given sunitinib were observed to resemble normal tissues. Conclusion: Sunitinib was shown to prevent histopathological changes in testicular tissue against ischemia/reperfusion damage. © 2021 Asociación Española de Andrología, Medicina Sexual y Reproductiva
dc.identifier.doi10.1016/j.androl.2020.10.001
dc.identifier.endpageS23
dc.identifier.issn1698-031X
dc.identifier.pmid34172383
dc.identifier.scopus2-s2.0-85108508380
dc.identifier.startpageS17
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/12741
dc.identifier.volume20
dc.identifier.wosWOS:000872142300003
dc.language.isoen
dc.publisherEdiciones Doyma, S.L.
dc.relation.ispartofRevista Internacional de Andrologia
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAntineoplastics drugs
dc.subjectIschemia/reperfusion
dc.subjectSunitinib
dc.subjectTestis
dc.subjectTorsion–detorsion
dc.subjectAnimals
dc.subjectGlutathione
dc.subjectHumans
dc.subjectIschemia
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectNF-kappa B
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReperfusion
dc.subjectReperfusion Injury
dc.subjectSaline Solution
dc.subjectSexually Transmitted Diseases
dc.subjectSolvents
dc.subjectSpermatic Cord Torsion
dc.subjectTumor Necrosis Factor-alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectmalonaldehyde
dc.subjectsolvent
dc.subjecttumor necrosis factor
dc.subjectanimal
dc.subjectcomplication
dc.subjecthuman
dc.subjectmetabolism
dc.titleEffect of sunitinib on testicular oxidative and proinflammatory damage induced by ischemia–reperfusion in rats; [Efecto de sunitinib en el daño oxidativo y proinflamatorio testicular inducido por isquemia-reperfusión en ratas]
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus5
rdl.citation.wos5
rdl.departmentErzincan Binali Yildirim University Faculty of Medicine, Department of Urology, Turkey. Electronic address: keskinerc@hotmail.com. | Erzincan Binali Yildirim University Faculty of Medicine, Department of Urology, Turkey. | Erzincan Binali Yildirim University Faculty of Medicine, Department of Pharmacology, Turkey. | Erzincan Binali Yildirim University Faculty of Medicine, Department of Histology and Embryology, Turkey. | Erzincan Binali Yildirim University Faculty of Medicine, Department of Anatomy, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)