Department of Biochemistry, University of New Mexico School of Medicine, Albuquerque 87131.
The mechanism that has been proposed for glyoxalase II [36] is summarized in Figure 3. It involves direct nucleophilic attack of an active-site histidine on the thiol ester substrate to form an acyl-imidazole intermediate which then rapidly hydrolyses. This is consistent with the known susceptibility of thiol esters to aminolysis and with the lability of acyl-imidazoles [47].