The oxidative disposition of potassium cyanide in mice

Abstract

The role of oxidative metabolism in the disposition of potassium cyanide (KCN), was investigated in mice administered KCN, (4.6 mg/kg, s.c.) containing 4.5 μCi [ 14C]KCN. The expired pulmonary metabolites, [ 14C]-hydrocyanic acid (HCN) and 14CO 2, were collected and analyzed. Approximately 1% and 2% of the KCN dose was expired as [ 14C]HCN and 14CO 2, respectively. Expiration of the pulmonary metabolites was decreased following pretreatment with sodium nitrite, sodium thiosulfate, oxygen, or a combination of cyanide antidotes. Treatment with hydrogen peroxide lowered the amount of [ 14C]HCN expired and did not alter the expiration of 14CO 2. Treatment with 3-amino-1,2,4-triazole (catalase inhibitor), superoxide dismutase, or diethyldithiocarbamic acid (superoxide dismutase inhibitor) did not change the amount of [ 14C]HCN expired. However, superoxide dismutase significantly increased the amount of 14CO 2 expired, whereas diethyldithiocarbamic acid decreased 14Co 2 expiration. The results from these studies suggest that in vivo cyanide can be oxidized to CO 2 and treatment with agents that alter availability of endogenous superoxide and/or hydrogen peroxide can alter the rate of cyanide oxidation.