International Journal of Bio-Science and Bio-Technology (IJBSBT) ISSN: 2233-7849 Vol-11-Issue-9-September-2019 Page | 157 Cyanide Toxicity: The Good, the Bad and the Ugly Emmanuel O. Ogbuagu 1* , Augustine I. Airaodion 2 , Victor N. Okoroukwu 3 , Uloaku Ogbuagu 4 and John A. Ekenjoku 5 1,5 Department of Pharmacology and Therapeutics, Abia State University, Uturu, Nigeria* 2,4 Department of Biochemistry, Federal University of Technology, Owerri, Imo State, Nigeria 3 Department of Pharmacology and Therapeutics, Gregory University Uturu, Abia State, Nigeria Corresponding Author: emma_onye2@yahoo.com ABSTRACT Cyanide toxicity occurs when a living organism is exposed to a compound that produces cyanide ion (CN - ) when dissolved in water. 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. Historically, cyanide has been used as a chemical warfare agent, and it could potentially be an agent for a terrorist attack. 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. 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. Management of cyanide toxicity involves air way control, ventilation and 100% oxygen, crystalloids and vasopressor, as needed for hypertension, Sodium bicarbonate is titrated according to arterial blood gas (ABG) and serum bicarbonate level; decontaminate the patient with removal of clothing /skin flushing and/or activated charcoal (1g/kg), as appropriate in alert patients or after endotracheal intubation in an unconscious patient through a nasogastric tube after gastric lavage. Administer hydroxocobalamin or sodium thiosulphate and sodium nitrite if the diagnosis is strongly suspected. Do not wait for laboratory confirmation. Therapeutic abortion may be indicated in the presence of fetal demise following obstetric evaluation and stabilization of the mother. Keywords: Cyanide Ion, Toxicity, Cytochrome Oxidase, Bradycardia 1. INTRODUCTION Cyanide poisoning occurs when a living organism is exposed to a compound that produces cyanide ions (CN − ) when dissolved in water. Common poisonous cyanide compounds include hydrogen cyanide gas and the crystalline solids potassium cyanide and sodium cyanide. The cyanide ion halts cellular respiration by inhibiting the enzyme cytochrome c oxidase found in the mitochondria. Cyanide toxicity is generally considered to be a rare form of poisoning. However, cyanide exposure occurs relatively frequently in patients with smoke inhalation from residential or industrial fires. In addition, intensive treatment with sodium nitroprusside or long-term consumption of cyanide- containing foods is a possible source of cyanide poisoning. Historically, cyanide has been used as a chemical warfare agent, and it could potentially be an agent for a terrorist attack [1,2]