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Hydrogen sulfide ameliorates zinc-induced cell death in neuroblastoma SH-SY5Y cells.

Free Radical Research 2017 December
Previous reports have demonstrated that excess zinc (Zn2+ ) released from nerve terminals following cerebral ischemia causes brain injury. Therefore, the disturbance of Zn2+ homeostasis in the brain is thought to be closely linked to neurotoxicity. Recently, hydrogen sulfide (H2 S), a gaseous mediator, has been reported to ameliorate ischemic brain injury. However, its mechanism is not fully understood. In this study, we examined whether sodium hydrogen sulfide (NaHS), an H2 S donor, protects against Zn2+ cytotoxicity using human neuroblastoma SH-SY5Y cells. NaHS dose-dependently prevented cell death caused by Zn2+ exposure. Treatment of cells with NaHS just before Zn2+ exposure exerted the most potent protection. Zn2+ induced loss of intracellular NAD+ and ATP and mitochondrial dysfunctions, resulting in cytotoxicity associated with failure of energy production; however, NaHS prevented these Zn2+ -induced events. In addition, NaHS suppressed Zn2+ -dependent activation of metal-responsive transcription factor-1 and induction of metallothionein gene expression. Zn2+ imaging with the Zn2+ -specific fluorescent indicator FluoZin-3 revealed that NaHS abolished the elevation of intracellular Zn2+ levels after Zn2+ exposure. These results suggest that entry of Zn2+ into cells was suppressed by NaHS. The measurement of H2 S derived from NaHS by o-fluorinated-azido-capped rhodamine (Rho-N3 F2 ), a reaction-based H2 S probe, revealed that H2 S levels in aqueous solutions were markedly reduced in the presence of Zn2+ . This finding suggests the possibility that H2 S reacts directly with Zn2+ and decreases extracellular Zn2+ levels. Taken together, we conclude that the protection of NaHS against Zn2+ cytotoxicity is exerted by inhibiting entry of Zn2+ into SH-SY5Ycells.

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