Clinical features include: initial bradycardia and hypertension, then transient tachypnea, cherry red skin, sooth in the mouth, normal or dilated pupils, diaphoresis, altered mental status, mydriasis, ataxia, generalized convulsions and coma. Cyanide toxicity occurs when cyanide attaches itself to ubiquitous metalloenzymes, rendering cytochrome oxidase inactive, thereby uncoupling mitochondrial oxidase phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen stores, consequently affecting tissues (brain and heart) with the highest oxygen requirement. Historically, cyanide has been used as a chemical warfare agent, and it could potentially be an agent for a terrorist attack.
Although, a rare form of poisoning, smoke inhalation, suicidal ingestion, industrial exposure, treatment with sodium nitroprusside, long term consumption of cyanide containing foods like apricot, poorly processed cassava, and apple seeds are possible sources of cyanide poisoning. It is argued that antagonism of sulfide inhibition of cytochrome c oxidase by NO is the crucial antidotal activity of nitrite rather than formation of methemoglobin.Ĭyanide toxicity occurs when a living organism is exposed to a compound that produces cyanide ion (CN-) when dissolved in water. Behavioral experiments testing the ability of mice to maintain balance on a rotating cylinder showed no motor impairment up to 24 h post sulfide exposure.
Compared to cyanide-intoxicated mice, animals surviving sulfide intoxication exhibited very short knockdown times (if any) and full recovery was extremely fast (∼15 min) irrespective of whether sodium nitrite was administered. Sulfide-intoxicated mice were neither helped by the supplemental administration of 100% oxygen nor were there any detrimental effects.
Nitrite anion was shown to rapidly produce NO in the bloodstream, as judged by the appearance of EPR signals attributable to nitrosylhemoglobin and methemoglobin, together amounting to less than 5% of the total hemoglobin present. However, sodium nitrite administered after the toxicant dose did not detectably ameliorate sulfide toxicity in this fast-delivery, single-shot experimental paradigm. Sodium nitrite, if given prophylactically to Swiss Webster mice, was shown to be highly protective against the acute toxic effects of sodium hydrosulfide (∼LD40 dose) with both agents administered by intraperitoneal injections. There are currently no FDA-approved antidotes for H2S/sulfide intoxication.
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