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    S-Sulfocysteine's toxic effects on HT-22 cells are not triggered by glutamate receptors, nor do they involve apoptotic or genotoxicity mechanisms
    (Springer, 2025) Tekin, Volkan; Altintas, Fatih; Oymak, Burak; Unal, Egem Burcu; Tunc-Ata, Melek; Elmas, Levent; Kucukatay, Vural
    S-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.