Fluvastatin attenuates doxorubicin-induced testicular toxicity in rats by reducing oxidative stress and regulating the blood-testis barrier via mTOR signaling pathway

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dc.contributor.authorGurel, Cevik
dc.contributor.authorKuscu, Gokce Ceren
dc.contributor.authorBuhur, Aylin
dc.contributor.authorDagdeviren, Melih
dc.contributor.authorOltulu, Fatih
dc.contributor.authorYavasogiu, Nefise Ulku Karabay
dc.contributor.authorYavasoglu, Altug
dc.date.accessioned2019-10-27T09:42:44Z
dc.date.available2019-10-27T09:42:44Z
dc.date.issued2019
dc.departmentEge Üniversitesien_US
dc.description.abstractDoxorubicin (DOX) is an anthracycline derivative antibiotic that still frequently used in the treatment of solid tumors and hematological malignancies. The clinical use of DOX is largely restricted due to acute and chronic renal, cardiac, hematological, and testicular toxicities. Previous studies have indicated that oxidative stress, lipid peroxidation, and apoptosis in germ cells are the main factors in DOX-induced testicular toxicity, but the entire molecular mechanisms that responsible for DOX-induced testicular damage are not yet fully understood. Fluvastatin is a cholesterol-lowering agent that acts by inhibiting hydroxylmethyl glutaryl coenzyme A, the key enzyme for cholesterol biosynthesis. In addition to its cholesterol-lowering effect, fluvastatin showed an antioxidant effect by cleaning hydroxyl and superoxide radicals and this drug could have a protective effect by acting on the mammalian target of rapamycin (mTOR) signal pathway in testicular damage caused by obesity. This study aimed to investigate the possible protective and therapeutic effects of fluvastatin on the DOX-induced testicular toxicity model by histochemical, immunohistochemical, biochemical, and real-time polymerase chain reaction analyses. The present study indicates that fluvastatin may have a protective and therapeutic effect by removing reactive oxygen species and by regulating the mTOR, connexin 43, and matrix metalloproteinase 9 protein and messenger ribonucleic acid expressions, which play an important role in regulating the blood-testis barrier. On the other hand, the use of fluvastatin as a protective/prophylactic agent was found to be more effective than the use of this drug for treatment. In light of this information, fluvastatin may be a candidate agent that can be used to prevent testicular toxicity observed in men receiving DOX treatment.en_US
dc.identifier.doi10.1177/0960327119862006
dc.identifier.endpage1343en_US
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.issue12en_US
dc.identifier.startpage1329en_US
dc.identifier.urihttps://doi.org/10.1177/0960327119862006
dc.identifier.urihttps://hdl.handle.net/11454/28806
dc.identifier.volume38en_US
dc.identifier.wosWOS:000476222300001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.language.isoenen_US
dc.publisherSage Publications Ltden_US
dc.relation.ispartofHuman & Experimental Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDoxorubicinen_US
dc.subjectfluvastatinen_US
dc.subjectgonadotoxicityen_US
dc.subjectmTORen_US
dc.titleFluvastatin attenuates doxorubicin-induced testicular toxicity in rats by reducing oxidative stress and regulating the blood-testis barrier via mTOR signaling pathwayen_US
dc.typeArticleen_US

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