<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-19T01:56:25Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12741" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12741</identifier><datestamp>2026-10-18T21:13:26Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>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]</dc:title><dc:creator>Keskin, Ercument</dc:creator><dc:creator>Erdogan, Abdullah</dc:creator><dc:creator>Suleyman, Halis</dc:creator><dc:creator>Yazici, Gulce Naz</dc:creator><dc:creator>Sunar, Mukadder</dc:creator><dc:creator>Gul, Mehmet Ali</dc:creator><dc:subject>Antineoplastics drugs</dc:subject><dc:subject>Ischemia/reperfusion</dc:subject><dc:subject>Sunitinib</dc:subject><dc:subject>Testis</dc:subject><dc:subject>Torsion–detorsion</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Humans</dc:subject><dc:subject>Ischemia</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>NF-kappa B</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Reperfusion</dc:subject><dc:subject>Reperfusion Injury</dc:subject><dc:subject>Saline Solution</dc:subject><dc:subject>Sexually Transmitted Diseases</dc:subject><dc:subject>Solvents</dc:subject><dc:subject>Spermatic Cord Torsion</dc:subject><dc:subject>Tumor Necrosis Factor-alpha</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>solvent</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>animal</dc:subject><dc:subject>complication</dc:subject><dc:subject>human</dc:subject><dc:subject>metabolism</dc:subject><dc:description>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 &lt; 0.001). Nuclear factor kappa B values, revealing a statistically significant difference between the TTD and STD groups (p &lt; 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 &lt; 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:description><dc:publisher>Ediciones Doyma, S.L.</dc:publisher><dc:date>2022</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/12741</dc:identifier><dc:identifier>https://doi.org/10.1016/j.androl.2020.10.001</dc:identifier><dc:identifier>1698-031X</dc:identifier><dc:language>en</dc:language><dc:relation>Revista Internacional de Andrologia</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/12741</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>