N-acetylcysteine attenuates sodium arsenite-induced oxidative stress and apoptosis in embryonic fibroblast cells

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dc.authorid0000-0002-4338-4687
dc.authorid0000-0002-2632-3516
dc.contributor.authorTasci, Tunahan
dc.contributor.authorOrta-Yilmaz, Banu
dc.contributor.authorAydin, Yasemin
dc.contributor.authorCaliskan, Mahmut
dc.date.accessioned2026-04-04T18:55:49Z
dc.date.available2026-04-04T18:55:49Z
dc.date.issued2024
dc.departmentİstanbul Bilgi Üniversitesi
dc.description.abstractIn recent years, the increase in environmental pollutants has been one of the most important factors threatening human and environmental health. Arsenic, a naturally occurring element found in soil, water, and air, easily enters the human body and leads to many metabolic disorders. In this study, we focused on the possible protective effects of N-acetylcysteine (NAC) against sodium arsenite (As)-induced toxic effects on embryonic fibroblast cells. The effects of As and NAC treatment on cells were evaluated, including cytotoxicity, oxidative stress, and apoptosis. Embryonic fibroblast cells were exposed to As (ranging from 0.01 mu M to 10 mu M) and NAC (at a concentration of 2 mM) for 24 h. The assessment of cytotoxicity markers, such as cell viability and lactate dehydrogenase (LDH), showed that As significantly reduced cell viability and increased LDH levels. Furthermore, we observed that As increased the amount of reactive oxygen species (ROS) in the cell, decreased the activity of antioxidant enzymes, and triggered apoptosis in cells. Additionally, our research revealed that the administration of NAC mitigates the detrimental effects of As. The results showed that As exerted hazardous effects on embryonic fibroblast cells through the induction of oxidative stress and apoptosis. In this context, our study provides evidence that NAC may have a protective effect against the toxicity of As in embryonic fibroblast cells.
dc.description.sponsorshipIstanbul University Scientific Research Projects [32513]
dc.description.sponsorshipThis study was supported by the Istanbul University Scientific Research Projects (Project No. 32513). Thanks to Istanbul Bilgi University for proofreading the article.
dc.identifier.doi10.1093/toxres/tfae128
dc.identifier.doi10.1093/toxres/tfae128
dc.identifier.issn2045-452X
dc.identifier.issn2045-4538
dc.identifier.issue4
dc.identifier.pmid39139367
dc.identifier.scopus2-s2.0-85201147520
dc.identifier.scopusqualityQ3
dc.identifier.urihttps://doi.org/10.1093/toxres/tfae128
dc.identifier.urihttps://hdl.handle.net/11411/10564
dc.identifier.volume13
dc.identifier.wosWOS:001290789400001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherOxford Univ Press
dc.relation.ispartofToxicology Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260402
dc.snmzKA_Scopus_20260402
dc.subjectN-Acetylcysteine
dc.subjectSodium Arsenite
dc.subjectOxidative Stress
dc.subjectApoptosis
dc.subjectEmbryonic Fibroblast Cells
dc.titleN-acetylcysteine attenuates sodium arsenite-induced oxidative stress and apoptosis in embryonic fibroblast cells
dc.typeArticle

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