Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF-Induced Testicular Toxicity

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dc.authoridSAG, sevda/0000-0001-8258-7324
dc.authoridAYNA, ADNAN/0000-0001-6801-6242
dc.authoridKUCUKLER, Sefa/0000-0002-8222-5515
dc.contributor.authorEmre Kizil, Hamit
dc.contributor.authorGur, Cihan
dc.contributor.authorAyna, Adnan
dc.contributor.authorDarendelioglu, Ekrem
dc.contributor.authorKucukler, Sefa
dc.contributor.authorSag, Sevda
dc.date.accessioned2024-10-04T18:49:24Z
dc.date.available2024-10-04T18:49:24Z
dc.date.issued2023
dc.departmentBayburt Üniversitesien_US
dc.description.abstractThe ameliorative effects of hesperidin (HES) on the toxicities created by sodium fluoride (NaF) in the testes tissue of rats were studied via oxidative stress, apoptosis and endoplasmic reticulum (ER) stress pathways. The animals were divided into five distinct groups (7 rats in each group). Group 1 was control group, group 2 received NaF-only (600 ppm), group 3 received HES-only (200 mg/kg bw); group 4 received NaF (600 ppm)+HES (100 mg/kg bw) and group 5 received NaF (600 ppm)+HES (200 mg/kg bw) for 14 days. NaF-induced testes tissue damage by reducing activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and levels of glutathione (GSH), and increasing lipid peroxidation levels. NaF treatment significantly downregulated the mRNA levels of SOD1, CAT and GPx. NaF supplementation caused apoptosis in the testes by upregulating p53, NFkB, caspase-3, caspase-6, caspase-9, and Bax and downregulating Bcl-2. Furthermore, NaF caused ER stress via increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. NaF treatment led to autophagy via upregulation of Beclin1, LC3A, LC3B and AKT2. In testes tissue, however, co-treatment with HES at doses of 100 and 200 mg/kg significantly reduced oxidative stress, apoptosis, autophagy and ER stress. Overall, the findings of this study suggest that HES may help to reduce testes damage caused by NaF toxicity.en_US
dc.identifier.doi10.1002/cbdv.202200982
dc.identifier.issn1612-1872
dc.identifier.issn1612-1880
dc.identifier.issue3en_US
dc.identifier.pmid36808882en_US
dc.identifier.scopus2-s2.0-85149315478en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/cbdv.202200982
dc.identifier.urihttp://hdl.handle.net/20.500.12403/3116
dc.identifier.volume20en_US
dc.identifier.wosWOS:000942880300001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWiley-V C H Verlag Gmbhen_US
dc.relation.ispartofChemistry & Biodiversityen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjecthesperidinen_US
dc.subjectsodium fluoride toxicityen_US
dc.subjectrat testicular tissueen_US
dc.subjectendoplasmic reticulum stressen_US
dc.subjectapoptosisen_US
dc.titleContribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF-Induced Testicular Toxicityen_US
dc.typeArticleen_US

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