S-Sulfocysteine's toxic effects on HT-22 cells are not triggered by glutamate receptors, nor do they involve apoptotic or genotoxicity mechanisms

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dc.authoridUNAL, EGEM BURCU/0000-0002-9499-2316
dc.authoridAltintas, Fatih/0000-0001-8779-0110
dc.contributor.authorTekin, Volkan
dc.contributor.authorAltintas, Fatih
dc.contributor.authorOymak, Burak
dc.contributor.authorUnal, Egem Burcu
dc.contributor.authorTunc-Ata, Melek
dc.contributor.authorElmas, Levent
dc.contributor.authorKucukatay, Vural
dc.date.accessioned2025-03-20T09:51:20Z
dc.date.available2025-03-20T09:51:20Z
dc.date.issued2025
dc.departmentİzmir Bakırçay Üniversitesi
dc.description.abstractS-Sulfocysteine (SSC) is a metabolite derived from the metabolism of sulfur-containing amino acids. It has been implicated in neurotoxicity observed in children with sulfite oxidase deficiency. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity. Based on the viability graph obtained following increasing concentrations of SSC, we determined the LC50 dose of SSC to be 125 mu M by probit analysis. The cytotoxic effects of SSC were not reversed by glutamate receptor blocker administration. However, SSC treatment did not induce caspase-3 activation or induce DNA damage. Our results showed that SSC has a cytotoxic effect on neurons like glutamate, but glutamate receptor blockers reversed glutamate-induced toxicity, while these blockers did not protect neurons from SSC toxicity. The absence of caspase-3 activation and DNA fragmentation, which are indicative of apoptosis, in SSC-induced cell death suggests that alternative cell death pathways, such as necrosis and oxytosis may be implicated. Further research is necessary to fully elucidate SSC-induced cell death. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity.
dc.description.sponsorshipPamukkale niversitesi
dc.description.sponsorshipThis study was a part of the PhD thesis of Volkan Tekin.
dc.identifier.doi10.1007/s10616-024-00697-0
dc.identifier.issn0920-9069
dc.identifier.issn1573-0778
dc.identifier.issue1
dc.identifier.pmid39749013
dc.identifier.scopus2-s2.0-85213811381
dc.identifier.scopusqualityQ3
dc.identifier.urihttps://doi.org/10.1007/s10616-024-00697-0
dc.identifier.urihttps://hdl.handle.net/20.500.14034/2490
dc.identifier.volume77
dc.identifier.wosWOS:001386425800001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofCytotechnology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250319
dc.subjectS-Sulphocysteine
dc.subjectCytotoxicity
dc.subjectHT-22 cell
dc.subjectApoptosis
dc.titleS-Sulfocysteine's toxic effects on HT-22 cells are not triggered by glutamate receptors, nor do they involve apoptotic or genotoxicity mechanisms
dc.typeArticle

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