Cellular toxicity of zinc can be attenuated by sodium hydrogen sulfide in neuronal SH-SY5Y cell

BackgroundsAlthough zinc acts as a major regulator of neuronal physiology, its dyshomeostasis may cause neuronal cell death. Hydrogen sulfide (H2S) has been reported to attenuate ischemic brain injury and to suppress Zn2+-induced neuronal cell death, but the underlying mechanisms have not been elucidated.MethodsWe determined the direct Zn2+-chelating capacity of sodium hydrogen sulfide (NaHS), an H2S donor, using specific Zn2+ fluorescent dyes (Zinpyr-1 and Zinquin) in SH-SY5Y cells.ResultsNaHS significantly suppressed the Zn2+-mediated increase in the fluorescence intensities of Zinpyr- 1 and Zinquin in a dose-dependent manner. NaHS significantly inhibited cell death induced by extracellular or intracellular Zn2+ overload. Furthermore, Zn2+-mediated increases in the phosphorylation of glycogen synthase kinase-3 and protein kinase C were highly suppressed by NaHS treatment.ConclusionThese results demonstrate that NaHS has the capacity to chelate extracellular and intracellular Zn2+, and could therefore be used in the protection against Zn2+ neurotoxicity.