Hydrogen peroxide utilization in myeloperoxidase-deficient leukocytes: a possible microbicidal control mechanism.
Phagocytosis-induced formate and glucose C-1 oxidation by the polymorphonuclear leukocytes of a patient with hereditary myeloperoxidase deficiency was considerably greater than normal. The addition of catalase to the leukocyte suspension was required for optimum formate oxidation. Azide and cyanide increased glucose C-1 oxidation by normal leukocytes but had little or no effect on myeloperoxidase-deficient leukocytes suggesting that these agents normally stimulate glucose C-1 oxidation, in part, by inhibition of myeloperoxidase. It is suggested that the inhibition or absence of myeloperoxidase results in an increased utilization of H(2)O(2) in nonmyeloperoxidase-mediated H(2)O(2)-dependent reactions such as formate oxidation and hexose monophosphate pathway activation. The possibility of a microbicidal control mechanism in which a decrease in the microbicidal activity of myeloperoxidase is offset, in part, by an increase in the nonenzymatic microbicidal activity of H(2)O(2) is considered.
D001386:Azides / Q000494:pharmacology; D002245:Carbon Dioxide / Q000032:analysis; D002374:Catalase; D046508:Culture Techniques; D003486:Cyanides / Q000494:pharmacology; D003920:Diabetes Mellitus / Q000378:metabolism; D005561:Formates / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006600:Hexosephosphates / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism*; D007840:Latex; D007962:Leukocytes / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008661:Metabolism, Inborn Errors / Q000378:metabolism / Q000503:physiopathology*; D008863:Microspheres; D010084:Oxidation-Reduction; D010544:Peroxidases / Q000378:metabolism*; D010587:Phagocytosis
D001386:Azides; D003486:Cyanides; D005561:Formates; D006600:Hexosephosphates; D007840:Latex; D002245:Carbon Dioxide; D006861:Hydrogen Peroxide; D010544:Peroxidases; D002374:Catalase; D005947:Glucose