Phenylglyoxal H2O is a reagent specific for the modification of arginyl residues in proteins. The resulting arginine-phenylglyoxal adduct can lead to either suppression or induction of permeability transition, depending on the net charge and hydrogen bonding capacity of the adduct by both isolated mitochondria and mammalian cells. When mammalian cells were incubated with low concentrations of negatively charged phenylglyoxal derivatives, the addition of oligomycin caused a depolarization of the mitochondrial membrane potential[1]. Chloride exchange in resealed human erythrocyte ghosts can be irreversibly inhibited with phenylglyoxal. At 0 degrees C, inhibition is instantaneous and fully reversible, whereas at higher temperature in an alkaline extracellular medium, covalent binding of phenylglyoxal leads to an irreversible inhibition of the transport membranes system. The rate of modification of anion transport depends on phenylglyoxal concentration, pH, temperature, and the presence of anions and reversible inhibitors of the anion transport system in fashions[2]. Pretreatment of human neutrophils with 100 microgram phenylglyoxal/ml for 30 min at 37 degrees C resulted in almost complete inhibition of phagocytosis of opsonized zymosan. Phenylglyoxal can be used effectively in the bacterial-killing test of phagocytes to inhibit intracellular killing after an initial period of ingestion[3]. Chemical modification of the Ca(2+)-ATPase with phenylglyoxal, as a modifier of arginine residues, leads to an almost total loss of the ATPase activity[4].
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