Assessment of the effect of sodium tetraborate on oxidative stress, inflammation, and apoptosis in lead-induced nephrotoxicity

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dc.authoridbengu, aydin sukru/0000-0002-7635-4855
dc.authoridKELES, OMER FARUK/0000-0002-7869-5311
dc.authoridMELEK, SULE/0000-0002-0677-722X
dc.contributor.authorYaman, Turan
dc.contributor.authorAkkoyun, H. Turan
dc.contributor.authorAkkoyun, Mahire Bayramoglu
dc.contributor.authorKaragozoglu, Fatma
dc.contributor.authorMelek, Sule
dc.contributor.authorKeles, Omer Faruk
dc.contributor.authorBengu, Aydin Sukru
dc.date.accessioned2024-12-24T19:28:03Z
dc.date.available2024-12-24T19:28:03Z
dc.date.issued2024
dc.departmentSiirt Üniversitesi
dc.description.abstractExposure to Pb, a toxic heavy metal, is a risk factor for renal damage. Borax, an essential trace element in cellular metabolism, is a naturally occurring compound found in many foods. This study investigated the effects of sodium tetraborate (ST), a source of borax, on renal oxidative stress and inflammation in rats exposed to Pb. Wistar Albino rats (n = 24) were divided into four groups: Control (0.5 mL, i.p. isotonic), Pb (50 mg/kg/day/i.p.), ST (4.0 mg/kg/day/oral), and Pb + ST groups. At the end of the five-day experimental period, kidney tissue samples were obtained and analyzed. Histopathologically, the Pb-induced damage observed in the Pb group improved in the Pb + ST group. Immunohistochemically, Pb administration increased the expression of inducible nitric oxide synthase, cyclooxygenase-2, and caspase-3. When evaluated biochemically, Pb application inhibited catalase and glutathione peroxidase (GSH-Px) enzyme activities and activated superoxide dismutase enzyme activity. An increase in malondialdehyde levels was considered an indicator of damage. ST application increases glutathione peroxidase enzyme activity and decreased malondialdehyde levels. These results indicate that ST might play a protective role against Pb-induced renal damage via the upregulation of renal tissue antioxidants and cyclooxygenase-2, inducible nitric oxide synthase, and caspase-3 immunoexpression.
dc.identifier.doi10.1080/01480545.2024.2358067
dc.identifier.issn0148-0545
dc.identifier.issn1525-6014
dc.identifier.pmid38804252
dc.identifier.scopus2-s2.0-85194567522
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1080/01480545.2024.2358067
dc.identifier.urihttps://hdl.handle.net/20.500.12604/6906
dc.identifier.wosWOS:001233830300001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofDrug and Chemical Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241222
dc.subjectAntioxidants
dc.subjectcaspase-3
dc.subjectcyclooxygenase-2
dc.subjectinducible nitric oxide synthase
dc.subjectlead
dc.subjectsodium tetraborate
dc.titleAssessment of the effect of sodium tetraborate on oxidative stress, inflammation, and apoptosis in lead-induced nephrotoxicity
dc.typeArticle

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