Abstract
Cyanide poisoning can occur from industrial disasters, smoke inhalation from fire, food, and multiple other sources. Cyanide inhibits mitochondrial oxidative phosphorylation by blocking mitochondrial cytochrome oxidase, which in turn results in anaerobic metabolism and depletion of adenosine triphosphate in cells. Rapid administration of antidote is crucial for life saving insevere cyanide poisoning. Multiple antidotes are available for cyanide poisoning. The action mechanism of cyanide antidotes include formation of methemoglobin, production of less or notoxic complex, and sulfane sulfur supplementation. At present, the available antidotes are amylnitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin, 4-dimethylaminophenol, and dicobalt edetate. Amyl nitrite, sodium nitrite, and 4-dimethylaminophenol induce the formation of methemoglobin. Sodium thiosulfate supplies the sulfane sulfur molecule to rhodanese, allowing formation of thiocyanate and regeneration of native enzymes. Hydroxocobalamin binds cyaniderapidly and irreversibly to form cyanocobalamin. Dicobalt edetate acts as a chelator of cyanide, forming a stable complex. Based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning. Amyl nitrite and sodium nitrite, which induce methemoglobin, should be avoided in victims of smoke inhalation because of serious adverse effects.
| Original language | English |
|---|---|
| Pages (from-to) | 1076-1083 |
| Number of pages | 8 |
| Journal | Journal of the Korean Medical Association |
| Volume | 56 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - 2013 Dec 1 |
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Keywords
- Cyanide
- Cyanide antidote
- Hydroxocobalamin
- Sodium thiosulfate
ASJC Scopus subject areas
- Medicine(all)
Cite this
Antidotes of cyanide intoxication. / Lee, Sung Woo; Kim, Jun Sik.
In: Journal of the Korean Medical Association, Vol. 56, No. 12, 01.12.2013, p. 1076-1083.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Antidotes of cyanide intoxication
AU - Lee, Sung Woo
AU - Kim, Jun Sik
PY - 2013/12/1
Y1 - 2013/12/1
N2 - Cyanide poisoning can occur from industrial disasters, smoke inhalation from fire, food, and multiple other sources. Cyanide inhibits mitochondrial oxidative phosphorylation by blocking mitochondrial cytochrome oxidase, which in turn results in anaerobic metabolism and depletion of adenosine triphosphate in cells. Rapid administration of antidote is crucial for life saving insevere cyanide poisoning. Multiple antidotes are available for cyanide poisoning. The action mechanism of cyanide antidotes include formation of methemoglobin, production of less or notoxic complex, and sulfane sulfur supplementation. At present, the available antidotes are amylnitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin, 4-dimethylaminophenol, and dicobalt edetate. Amyl nitrite, sodium nitrite, and 4-dimethylaminophenol induce the formation of methemoglobin. Sodium thiosulfate supplies the sulfane sulfur molecule to rhodanese, allowing formation of thiocyanate and regeneration of native enzymes. Hydroxocobalamin binds cyaniderapidly and irreversibly to form cyanocobalamin. Dicobalt edetate acts as a chelator of cyanide, forming a stable complex. Based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning. Amyl nitrite and sodium nitrite, which induce methemoglobin, should be avoided in victims of smoke inhalation because of serious adverse effects.
AB - Cyanide poisoning can occur from industrial disasters, smoke inhalation from fire, food, and multiple other sources. Cyanide inhibits mitochondrial oxidative phosphorylation by blocking mitochondrial cytochrome oxidase, which in turn results in anaerobic metabolism and depletion of adenosine triphosphate in cells. Rapid administration of antidote is crucial for life saving insevere cyanide poisoning. Multiple antidotes are available for cyanide poisoning. The action mechanism of cyanide antidotes include formation of methemoglobin, production of less or notoxic complex, and sulfane sulfur supplementation. At present, the available antidotes are amylnitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin, 4-dimethylaminophenol, and dicobalt edetate. Amyl nitrite, sodium nitrite, and 4-dimethylaminophenol induce the formation of methemoglobin. Sodium thiosulfate supplies the sulfane sulfur molecule to rhodanese, allowing formation of thiocyanate and regeneration of native enzymes. Hydroxocobalamin binds cyaniderapidly and irreversibly to form cyanocobalamin. Dicobalt edetate acts as a chelator of cyanide, forming a stable complex. Based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning. Amyl nitrite and sodium nitrite, which induce methemoglobin, should be avoided in victims of smoke inhalation because of serious adverse effects.
KW - Cyanide
KW - Cyanide antidote
KW - Hydroxocobalamin
KW - Sodium thiosulfate
UR - http://www.scopus.com/inward/record.url?scp=84892632053&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84892632053&partnerID=8YFLogxK
U2 - 10.5124/jkma.2013.56.12.1076
DO - 10.5124/jkma.2013.56.12.1076
M3 - Review article
AN - SCOPUS:84892632053
VL - 56
SP - 1076
EP - 1083
JO - Journal of the Korean Medical Association
JF - Journal of the Korean Medical Association
SN - 1975-8456
IS - 12
ER -