Carvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite-induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats

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dc.authorid0000-0001-6775-7858
dc.authorid0000-0003-4450-6540
dc.authorid0000-0002-8457-9448
dc.authorid0000-0002-6250-5093
dc.authorid0000-0002-8490-2479
dc.contributor.authorGür, Cihan
dc.contributor.authorAkarsu, Serkan Ali
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorTuncer, Sibel Çiğdem
dc.date.accessioned2023-03-13T08:11:30Z
dc.date.available2023-03-13T08:11:30Z
dc.date.issued2023
dc.departmentTıp Fakültesi
dc.description.abstractArsenic (As) is a highly toxic metalloid. Carvacrol (CAR) is the active ingredient of Lamiaceae plants and has various biological and pharmacological properties. The present study investigated the protective effects of carvacrol (CAR) against testicular toxicity induced by sodium arsenite (SA). Rats were given SA (10 mg/kg) and/or CAR (25 or 50 mg/kg) for 14 days. Semen analyzes showed that CAR increased sperm motility and decreased the percentage of abnormal and dead sperm. It was determined that the oxidative stress induced by SA decreased with the increase of Nrf-2 and HO-1 expressions, SOD, CAT, GPx, and GSH levels, and MDA levels decreased after CAR treatment. It was observed that autophagy and inflammation triggered by SA in testicular tissue were alleviated by suppressing the expressions of LC3A, LC3B, MAPK-14, NF-?B, TNF-?, IL-1?, iNOS, and COX-2 biomarkers in rats given CAR. Also, CAR treatment suppressed SA-induced apoptosis by inhibiting Bax and Caspase-3 expressions in testicles and up-regulating Bcl-2 expression. Histopathological analyzes showed that rats given SA had deterioration in tubule structure and spermatogenesis cell line, especially a serious loss of spermatogonia cells, atrophy of seminiferous tubules, and deterioration of germinal epithelium. In the group given CAR, the germinal epithelium and connective tissue were in normal morphological structure and an increase in seminiferous tubule diameters was observed. As a result, it was determined that oxidative stress, inflammation, autophagy, and apoptosis induced by SA were suppressed by CAR, thus protecting the testicular tissue from damage and increasing semen quality.
dc.identifier.doi10.1002/tox.23762
dc.identifier.pmid36880177
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org/10.1002/tox.23762
dc.identifier.urihttps://hdl.handle.net/20.500.12451/10337
dc.identifier.wosWOS:000943943000001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofEnvironmental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectCarvacrol
dc.subjectOxidative Stress
dc.subjectSodium Arsenite
dc.subjectTesticular Toxicity
dc.titleCarvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite-induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats
dc.typeArticle

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