Captopril does not scavenge superoxide: captopril prevents O2-. production by chelating copper.
The purpose of this study was to use a direct method, that of electron spin resonance spectroscopy, to evaluate the ability of captopril, an angiotensin-converting enzyme inhibitor, to prevent the superoxide-mediated formation of phenyl radicals. Results indicate that, under certain conditions, captopril is a potent inhibitor of the generation of phenyl radicals, produced by the autoxidation of phenylhydrazine. The inhibitory effect of captopril, however, was better understood as a direct interaction of the drug with the metals that catalyze the autoxidation process rather than as a reaction of captopril with the free radicals generated. This last conclusion was supported by the finding that captopril was not able to inhibit the superoxide anion-mediated reduction of nitroblue tetrazolium.
Jay
D
D
Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, México City, México.
Cuéllar
A
A
Zamorano
R
R
Muñoz
E
E
Gleason
R
R
D002216:Captopril / Q000494:pharmacology*; D002614:Chelating Agents / Q000494:pharmacology*; D003300:Copper / Q000737:chemistry*; D004578:Electron Spin Resonance Spectroscopy; D016166:Free Radical Scavengers; D010084:Oxidation-Reduction / Q000187:drug effects; D010659:Phenylhydrazines / Q000737:chemistry; D013482:Superoxide Dismutase / Q000494:pharmacology; D013481:Superoxides / Q000737:chemistry* / Q000494:pharmacology
D002614:Chelating Agents; D016166:Free Radical Scavengers; D010659:Phenylhydrazines; C030299:phenylhydrazine; D013481:Superoxides; D003300:Copper; D002216:Captopril; D013482:Superoxide Dismutase