Carvacrol Reduces Mercuric Chloride-Induced Testicular Toxicity by Regulating Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histopathological Changes

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dc.authorid0000-0001-5573-4923
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorÖz, Mehmet
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2024-04-25T07:54:20Z
dc.date.available2024-04-25T07:54:20Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractMercuric chloride (HgCl2) is a heavy metal that is toxic to the human body. Carvacrol (CAR) is a flavonoid found naturally in plants and has many biological and pharmacological activities including anti-inflammatory, antioxidant, and anticancer activities. This study aimed to investigate the efficacy of CAR in HgCl2-induced testicular tissue damage. HgCl2 was administered intraperitoneally at a dose of 1.23 mg/kg body weight alone or in combination with orally administered CAR (25 mg/kg and 50 mg/kg body weight) for 7 days. Biochemical and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and autophagy pathways in testicular tissue. CAR treatment increased HgCl2-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels. In addition, CAR reduced MDA levels, a marker of lipid peroxidation. CAR decreased the levels of inflammatory mediators NF-?B, TNF-?, IL-1?, COX-2, iNOS, MAPK14, MAPK15, and JNK. The increases in apoptotic Bax and Caspase-3 with HgCl2 exposure decreased with CAR, while the decreased antiapoptotic Bcl-2 level increased. CAR reduced HgCl2-induced autophagy damage by increasing Beclin-1, LC3A, and LC3B levels. Overall, the data from this study suggested that testicular tissue damage associated with HgCl2 toxicity can be mitigated by CAR administration.
dc.identifier.doi10.1007/s12011-023-04022-2
dc.identifier.issn0163-4984
dc.identifier.pmid38133725
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org10.1007/s12011-023-04022-2
dc.identifier.urihttps://hdl.handle.net/20.500.12451/11711
dc.identifier.wosWOS:001130310600002
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofBiological Trace Element Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectCarvacrol
dc.subjectInflammation
dc.subjectMercuric Chloride
dc.subjectOxidative Stress
dc.subjectTesticular Toxicity
dc.titleCarvacrol Reduces Mercuric Chloride-Induced Testicular Toxicity by Regulating Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histopathological Changes
dc.typeArticle

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