Klebanoff S J, Pincus S H
J Clin Invest. 1971 Oct;50(10):2226-9. doi: 10.1172/JCI106718.
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.
遗传性髓过氧化物酶缺乏症患者的多形核白细胞通过吞噬作用诱导的甲酸盐和葡萄糖C-1氧化明显高于正常水平。为了实现最佳的甲酸盐氧化，需要向白细胞悬液中添加过氧化氢酶。叠氮化物和氰化物可增加正常白细胞的葡萄糖C-1氧化，但对髓过氧化物酶缺乏的白细胞几乎没有影响，这表明这些试剂通常部分通过抑制髓过氧化物酶来刺激葡萄糖C-1氧化。有人提出，髓过氧化物酶的抑制或缺失会导致在非髓过氧化物酶介导的依赖H2O2的反应（如甲酸盐氧化和己糖磷酸途径激活）中H2O2的利用率增加。人们考虑了一种杀菌控制机制的可能性，即髓过氧化物酶杀菌活性的降低部分被H2O2非酶杀菌活性的增加所抵消。
