Effect of melatonin on testicular damage in streptozotocin-induced diabetes rats

dc.authorid0000-0002-2348-7427en_US
dc.contributor.authorGüneli, E.
dc.contributor.authorTuğyan, K.
dc.contributor.authorÖztürk, Hülya
dc.contributor.authorGümüştekin, M.
dc.contributor.authorCilaker, Serap
dc.contributor.authorUysal, N.
dc.date.accessioned2021-06-23T19:25:58Z
dc.date.available2021-06-23T19:25:58Z
dc.date.issued2008
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractBackground: It is well known that diabetes mellitus is associated with impairment of testicular function. In the present study, we aimed to demonstrate the effect of melatonin on testicular damage in male rats with streptozotocin (STZ)-induced diabetes. Methods: Male Wistar rats were divided into 4 groups: (1) control group, (2) melatonin-treated nondiabetic group, (3) diabetic group and (4) melatonin-treated diabetic group. Diabetes was induced by STZ injection. Melatonin was administered intraperitoneally at the dose of 10 mg/kg for 5 days. Testicular damage was examined by using hematoxylin and eosin staining and periodic acid-Schiff staining, and apoptosis was determined by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). Potential disorders associated with seminiferous tubular sperm formation were evaluated using the Johnsen score. Results: Diabetic rats showed a reduction in seminiferous tubule diameter, increased thickening of the basement membrane in seminiferous tubules and degenerated germ cells. TUNEL-positive cells were significantly more numerous in diabetic rats than in control rats. Melatonin significantly attenuated the diabetes-induced morphological changes and germ cell apoptosis in the diabetic rat testis. The number of polymorphonuclear leukocytes was signifi cantly decreased in group 4 when compared to group 3. Conclusions: These results suggest that intraperitoneal administration of melatonin for 5 days is a potentially beneficial agent to reduce testicular damage in adult diabetic rats, probably by decreasing oxidative stress. Copyright (C) 2008 S. Karger AG, Basel.en_US
dc.identifier.doi10.1159/000118032
dc.identifier.endpage360en_US
dc.identifier.issn0014-312X
dc.identifier.issn1421-9921
dc.identifier.issue4en_US
dc.identifier.pmid18303272en_US
dc.identifier.scopus2-s2.0-43949145970en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage354en_US
dc.identifier.urihttps://doi.org/10.1159/000118032
dc.identifier.urihttps://hdl.handle.net/20.500.12491/6351
dc.identifier.volume40en_US
dc.identifier.wosWOS:000254893000007en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorÖztürk, Hülya
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofEuropean Surgical Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDiabetic Testes Injuryen_US
dc.subjectMelatoninen_US
dc.subjectGerm Cell Apoptosisen_US
dc.subjectStreptozotocinen_US
dc.titleEffect of melatonin on testicular damage in streptozotocin-induced diabetes ratsen_US
dc.typeArticleen_US

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