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dc.contributor.authorÇiftel, Enver
dc.contributor.authorMercantepe, Tolga
dc.contributor.authorÇiftel, Serpil
dc.contributor.authorKarakaş, Sibel Mataracı
dc.contributor.authorAktepe, Rıza
dc.contributor.authorYılmaz, Adnan
dc.contributor.authorMercantepe, Filiz
dc.date.accessioned2025-07-28T12:39:55Z
dc.date.available2025-07-28T12:39:55Z
dc.date.issued2025en_US
dc.identifier.citationCiftel, E., Mercantepe, T., Ciftel, S., Karakas, S. M., Aktepe, R., Yilmaz, A., & Mercantepe, F. (2025). Somatostatin and N-acetylcysteine on testicular damage triggered by ischemia reperfusion: cellular protection and antioxidant effects. Hormones. https://doi.org/10.1007/s42000-025-00650-6en_US
dc.identifier.issn1109-3099
dc.identifier.urihttps://doi.org/10.1007/s42000-025-00650-6
dc.identifier.urihttps://hdl.handle.net/11436/10700
dc.description.abstractIschemia–reperfusion (I/R) injury is a significant cause of testicular damage, leading to infertility and other reproductive dysfunctions. Antioxidant therapies have emerged as a potential intervention to mitigate oxidative stress and cellular damage. This study investigates the effects of somatostatin (SST) and N-acetylcysteine (NAC) on testicular damage induced by I/R, focusing on their antioxidant and cellular protective effects. Twenty-four male rats were divided into four groups, as follows: sham operated, I/R injury, I/R + somatostatin treatment, and I/R + NAC treatment. A testicular I/R injury was induced surgically, followed by either SST or NAC administration. Testicular tissues were assessed histopathologically using hematoxylin and eosin staining and employing Johnson's biopsy scoring. Immunohistochemical analyses were performed for caspase- 3, 8-hydroxy- 2'-deoxyguanosine (8-OHdG), testis-specific histone 2B, and testosterone to evaluate apoptosis, oxidative DNA damage, cellular proliferation, and steroidogenesis, respectively. Serum levels of testosterone and follicle-stimulating hormone (FSH) were measured by biochemical analysis. The results showed that both SST and NAC treatments significantly ameliorated histopathological damage and reduced the levels of caspase- 3 and 8-OHdG, indicating reduced apoptosis and oxidative DNA damage. Furthermore, increased testis-specific histone 2B positivity suggested enhanced cellular proliferation. Notably, administration of SST decreased testosterone positivity in the testis, whereas NAC treatment increased it. However, no significant differences in serum testosterone levels were observed between the NAC and SST groups. In addition, serum FSH levels of the I/R + SST group were found to be significantly higher than those of the control group. SST and NAC exhibit protective effects against testicular damage induced by I/R, as evidenced by their antioxidant and anti-apoptotic properties. The differential impact on testosterone positivity in the testis tissue highlights distinct underlying mechanisms, warranting further investigation. Despite these promising findings, the lack of significant changes in serum hormone levels calls for additional studies to fully elucidate the therapeutic potential and mechanistic pathways of SST and NAC in the context of testicular I/R injury.en_US
dc.language.isoengen_US
dc.publisherSpringer Natureen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectIschemia–reperfusionen_US
dc.subjectN-acetylcysteineen_US
dc.subjectRaten_US
dc.subjectSomatostatinen_US
dc.subjectTestisen_US
dc.titleSomatostatin and N-acetylcysteine on testicular damage triggered by ischemia reperfusion: cellular protection and antioxidant effectsen_US
dc.typearticleen_US
dc.contributor.departmentRTEÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümüen_US
dc.contributor.institutionauthorMercantepe, Tolga
dc.contributor.institutionauthorKarakaş, Sibel Mataracı
dc.contributor.institutionauthorAkpete, Rıza
dc.contributor.institutionauthorYılmaz, Adnan
dc.contributor.institutionauthorMercantepe, Filiz
dc.identifier.doi10.1007/s42000-025-00650-6en_US
dc.relation.journalHormonesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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