Open AccessAntiarthritic drugs containing thiol groups scavenge hypochlorite and inhibit its formation by myeloperoxidase from human leukocytes. A therapeutic mechanism of these drugs in rheumatoid arthritis?
Author(s) -
Cuperus Roelck A.,
Muijsers Anton O.,
Wever Ron
Publication year - 1985
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780281106
Subject(s) - tiopronin , myeloperoxidase , penicillamine , pharmacology , rheumatoid arthritis , hypochlorite , chemistry , hypochlorous acid , thiol , arthritis , drug , mechanism of action , sodium hypochlorite , medicine , biochemistry , immunology , in vitro , inflammation , organic chemistry
We investigated the effect of antiarthritic drugs containing thiol groups, such as D‐penicillamine, tiopronin ( N ‐[2‐mercaptopropionyl]glycine), sodium aurothiomalate, and aurothioglucose, on the chlorinating activity of myeloperoxidase purified from human leukocytes. Hypochlorite, the reactive product of the reaction catalyzed by myeloperoxidase, was effectively scavenged by these antiarthritic drugs, and in addition, D‐penicillamine and tiopronin inhibited myeloperoxidase itself. The above‐mentioned effects of these drugs were observed at concentrations that occur in the serum of rheumatoid arthritis patients treated with these agents. We suggest that the therapeutic effect of these antiarthritic drugs may be due to the protection of tissues against the reactive HOCl released by activated granulocytes at inflamed sites.