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. 2016 Jul 21;1378(1):5–16. doi: 10.1111/nyas.13148

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© 2016 The Authors. Annals of the New York Academy of Sciences published by Wiley Periodicals, Inc. on behalf of New York Academy of Sciences.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Potential mechanisms of H₂S‐induced cytotoxicity. Hydrogen sulfide inhibits cytochrome c oxidase in mitochondria, leading to low ATP production. H₂S also disrupts calcium homeostasis, leading to high intracellular calcium. Depletion of reduced glutathione leads to generation of reactive oxygen species (ROS). H₂S induces DNA damage, persulfidation of protein and lipids, and dysregulation of ion channels, which are further aggravated by excessive intracellular levels of ROS. Collectively, these H₂S‐induced effects may lead to programmed cell death in neurons and glia.