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Studying the Efficacy of Antidotes for Metabolic Cyanide Poisoning
Author(s) -
Harrison M.,
Haines D. C.,
Petrikovics I.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb208
Subject(s) - cyanide , cyanide poisoning , chemistry , cytochrome c oxidase , thiosulfate , rhodanese , sodium thiosulfate , methemoglobin , sodium nitrite , antidote , thiocyanate , biochemistry , cytochrome c , electron acceptor , pharmacology , heme , sulfur , mitochondrion , enzyme , toxicity , hemoglobin , inorganic chemistry , organic chemistry , medicine
Cyanide is found in a variety of environmental and industrial sources. Cyanide inhibits mitochondrial cyctochrome c oxidase, the terminal electron acceptor in the electron transport chain, resulting in decreased oxidative metabolism and decreased oxygen utilization. The goal of our study was to test novel prophylactic and therapeutic treatments for their ability to protect against cyanide toxicity. Mice were treated with cyanide and various antidotes, and then brain mitochondria were isolated and the cytochrome c oxidase activity in the brain mitochondria determined. The antidotes tested were sulfur donors including dimethyltrisulfide, thiotaurate, and thiosulfate administered with exogenous rhodonase, an enzyme that uses sulfur donors to convert cyanide to much less toxic thiocyanate. Sodium nitrite, which oxidizes hemoglobin to methemoglobin which can sequester the cyanide, was also administered in the presence and absence of the novel therapeutics. The cytochrome c oxidase activity data complemented survival data in the determination of antidote efficacy.