A Comparison of the Cyanide-Scavenging Capabilities of Some Cobalt-Containing Complexes in Mice.

Four cobalt-containing macrocyclic compounds previously shown to ameliorate cyanide toxicity have been comparatively evaluated with an acute sublethal toxicity model in conscious (unanesthetized) adult male Swiss-Webster mice. All of the compounds (the cobalt-corrins cobalamin and cobinamide, a cobalt-porphyrin, plus a cobalt-Schiff base macrocycle) given 5 min prior to the toxicant dose significantly decreased the righting-recovery time of cyanide-intoxicated mice, but the doses required for maximal antidotal effect varied. Additionally, all of the compounds tested significantly reduced the righting-recovery time when administered at either 1 or 2 min after cyanide intoxication, but none of the compounds tested significantly reduced the righting-recovery time when delivered 5 min after the toxicant dose.

Cyanide Scavenging by a Cobalt Schiff-Base Macrocycle: A Cost-Effective Alternative to Corrinoids.

The complex of cobalt(II) with the ligand 2,12-dimethyl-3,7,11,17-tetraazabicyclo-[11.3.1]heptadeca-1(17)2,11,13,15-pentaene (CoN4[11.

The resistance of electron-transport chain Fe-S clusters to oxidative damage during the reaction of peroxynitrite with mitochondrial complex II and rat-heart pericardium.

The effects of peroxynitrite and nitric oxide on the iron-sulfur clusters in complex II (succinate dehydrogenase) isolated from bovine heart have been studied primarily by EPR spectroscopy and no measurable damage to the constitutive 2Fe-2S, 3Fe-4S, or 4Fe-4S clusters was observed. The enzyme can be repeatedly oxidized with a slight excess of peroxynitrite and then quantitatively re-reduced with succinate. When added in large excess, peroxynitrite reacted with at least one tyrosine in each subunit of complex II to form 3-nitrotyrosines, but activity was barely compromised.

Antagonism of nitric oxide toward the inhibition of cytochrome c oxidase by carbon monoxide and cyanide.

The principle mitochondrial target where the respiratory inhibitors CO, CN(-), and NO act in the execution of their acute toxic effects is complex IV of the electron-transport chain, cytochrome c oxidase. However, there is a paucity of studies in the literature regarding the concerted effects of such poisons. Accordingly, the combined inhibitory effects of CO + CN(-), NO + CN(-), and NO + CO on the activity of cytochrome c oxidase preparations are reported.