Reactive sulfur species: kinetics and mechanism of the reaction of hypothiocyanous acid with cyanide to give dicyanosulfide in aqueous solution.

The chief sources of cyanide (CN(-)) in humans are tobacco and occupationally derived smoke, inflammation [vis-a-vis myeloperoxidase (MPO)-induced chlorination of glycine], and microbial cyanogenesis (including Pseudomonas aeruginosa infection of the cystic fibrosis lung). The human mucosae of healthy individuals are usually protected from infection by innate defense mechanisms that include the defensive peroxidase systems. In the oral cavity, salivary peroxidase and MPO catalyze the oxidation of the pseudohalide thiocyanate (SCN(-)) by hydrogen peroxide to produce the antimicrobial hypothiocyanite (OSCN(-)). Lactoperoxidase carries out the same reaction in the human lung (as does MPO during inflammatory response). In the present study, we show that OSCN(-) and CN(-) react with pH-dependent kinetics to produce SCN(-) and cyanate (OCN(-)) via dicyanosulfide (NCSCN), with the maximum rate occurring near neutral, physiological pH. In addition to presenting a detailed chemical mechanism, we discuss unresolved issues, including the possible biological relevance of the NCSCN intermediate.