Attenuation of sodium arsenite-induced cardiotoxicity and neurotoxicity with the antioxidant, anti-inflammatory, and antiapoptotic effects of hesperidin

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dc.authoridKUZU, Muslum/0000-0002-1375-7673
dc.authoridcaglayan, cuneyt/0000-0001-5608-554X
dc.authoridKUCUKLER, Sefa/0000-0002-8222-5515
dc.contributor.authorKuzu, Muslum
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorYildirim, Serkan
dc.contributor.authorCaglayan, Cuneyt
dc.contributor.authorKucukler, Sefa
dc.date.accessioned2024-09-29T15:51:26Z
dc.date.available2024-09-29T15:51:26Z
dc.date.issued2021
dc.departmentKarabük Üniversitesien_US
dc.description.abstractIn the scope of the study, the protective effect of hesperidin (HES), a flavanone glycoside, was investigated against sodium arsenite (NaAsO2, SA) induced heart and brain toxicity. For this purpose, 35 Sprague-Dawley male rats were divided into 5 different groups, 7 in each group. Physiological saline was given to the first group. Dose of 200 mg/kg of HES to the second group, 10 mg/kg dose of SA to the 3rd group, 100 mg/kg HES and 10 mg/kg SA to the 4th group, 200 mg/kg HES, and 10 mg/kg SA to the 5th group were given orally for 15 days. At the end of the study, biochemical, histopathological, and immunohistochemical examinations were performed on the heart and brain tissues of the rats. According to the results, SA increased malondialdehyde (MDA) and 8-hydroxy-2 '-deoxyguanosine (8-OHdG) levels and decreased glutathione (reduced, GSH) level and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in both tissues. Also, it increased cardiac lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB (CK-MB) activities and cardiac troponin-I level (cTn-I), cerebral acetylcholine esterase activity, nuclear factor kappa-B (NF-kappa B), tumor necrosis factor-alpha (TNF-alpha), interleukin-one beta (IL-1 beta), and cysteine aspartate-specific protease-3 (caspase-3) levels. In addition, as a result of histopathological examination, it was determined that SA damaged tissue architecture, and as a result of immunohistochemical examination, it increased cardiac Bcl-2-associated X protein (Bax) and cerebral glial fibrillary acidic protein (GFAP) expression. The results have also shown that HES co-treatment has an antioxidant, anti-inflammatory, antiapoptotic effect on SA-induced toxicity and aids to protect tissue architecture by showing a regulatory effect on all values. Consequently, it was determined that HES co-treatment had a protective effect on SA-induced heart and brain toxicity in rats.en_US
dc.identifier.doi10.1007/s11356-020-11327-5
dc.identifier.endpage10831en_US
dc.identifier.issn0944-1344
dc.identifier.issn1614-7499
dc.identifier.issue9en_US
dc.identifier.pmid33099738en_US
dc.identifier.scopus2-s2.0-85093914717en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage10818en_US
dc.identifier.urihttps://doi.org/10.1007/s11356-020-11327-5
dc.identifier.urihttps://hdl.handle.net/20.500.14619/4077
dc.identifier.volume28en_US
dc.identifier.wosWOS:000582312400003en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer Heidelbergen_US
dc.relation.ispartofEnvironmental Science and Pollution Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSodium arseniteen_US
dc.subjectHesperidinen_US
dc.subjectCardiotoxicityen_US
dc.subjectNeurotoxicityen_US
dc.subjectAntioxidanten_US
dc.subjectInflammationen_US
dc.subjectApoptosisen_US
dc.titleAttenuation of sodium arsenite-induced cardiotoxicity and neurotoxicity with the antioxidant, anti-inflammatory, and antiapoptotic effects of hesperidinen_US
dc.typeArticleen_US

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