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Hydrogen Sulfide—Mechanisms of Toxicity and Development of an Antidote
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Journal Article
Hydrogen Sulfide—Mechanisms of Toxicity and Development of an Antidote
2016
Overview
Hydrogen sulfide is a highly toxic gas—second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known and no specific therapy exists for sulfide poisoning. We show in several cell types, including human inducible pluripotent stem cell (hiPSC)-derived neurons, that sulfide inhibited complex IV of the mitochondrial respiratory chain and induced apoptosis. Sulfide increased hydroxyl radical production in isolated mouse heart mitochondria and F
2
-isoprostanes in brains and hearts of mice. The vitamin B
12
analog cobinamide reversed the cellular toxicity of sulfide and rescued
Drosophila melanogaster
and mice from lethal exposures of hydrogen sulfide gas. Cobinamide worked through two distinct mechanisms: direct reversal of complex IV inhibition and neutralization of sulfide-generated reactive oxygen species. We conclude that sulfide produces a high degree of oxidative stress in cells and tissues and that cobinamide has promise as a first specific treatment for sulfide poisoning.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/106
/ 13/2
/ 64
/ 64/24
/ 64/60
/ Animals
/ Electron Transport Complex IV - metabolism
/ F2-Isoprostanes - antagonists & inhibitors
/ F2-Isoprostanes - metabolism
/ Humanities and Social Sciences
/ Humans
/ Hydrogen Sulfide - antagonists & inhibitors
/ Hydroxyl Radical - antagonists & inhibitors
/ Hydroxyl Radical - metabolism
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - drug effects
/ Induced Pluripotent Stem Cells - metabolism
/ Male
/ Mice
/ Mitochondria, Heart - drug effects
/ Mitochondria, Heart - metabolism
/ Potassium Cyanide - antagonists & inhibitors
/ Potassium Cyanide - toxicity
/ Rats
/ Rodents
/ Science
/ Sulfides
/ Sulfides - antagonists & inhibitors
/ Toxicity
