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KMID : 1034820180140040425
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Molecular & Cellular Toxicology
2018 Volume.14 No. 4 p.425 ~ p.436
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Cellular toxicity of zinc can be attenuated by sodium hydrogen sulfide in neuronal SH-SY5Y cell
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Lee Sung-Ryul
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Abstract
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Backgrounds: Although 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.
Methods: We 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.
Results: NaHS 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-3β and protein kinase C were highly suppressed by NaHS treatment.
Conclusion: These results demonstrate that NaHS has the capacity to chelate extracellular and intracellular Zn2+, and could therefore be used in the protection against Zn2+ neurotoxicity.
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KEYWORD
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Hydrogen sulfide, SH-SY5Y, Zinc, Cell death, Zinquin, Zinpyr-1, Chelation, Glycogen synthase kinase-3β, Neutral red uptake
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