Kovalenko E I, Semenkova G N, Cherenkevich S N
Tsitologiia. 2007;49(10):839-47.
The influence of H2O2 at concentrations of 10(-8)--10(-2) mol/l on neutrophil ability to generate the reactive oxygen and chlorine species (ROCS) and secrete myeloperoxidase (MPO) was studied, and H202 injurious effect on neutrophils was also investigated in this work. It was revealed that H2O2 at concentrations of 2 x 10(-3)--2 x 10(-2) mol/l induced disturbance of the neutrophil membrane barrier properties and lactate dehydrogenase release. The incubation of the neutrophils with the addition of 10(-4)--10(-7) mol/l H2O2 led to an increase in the cell ability to generate ROCS during phagocytosis and decreased neutrophil ability to secrete MPO and ROCS in extracellular medium during adhesion. The mechanisms of H2O2 effect are coupled with arachidonic acid metabolism. Inhibition of metabolic pathways of 5-lipoxygenase or cyclooxygenase increased the destructive effect of H2O2 on the cells. Five-lipoxygenase way prohibition led to cancellation of H2O2 influence on MPO and ROCS secretion and to enhancement of H2O2 effect on neutrophil ability to generate ROCS during phagocytosis. The data obtained testify to the high neutrophil resistance to destructive effect of H2O2 and confirm the regulatory role of H2O2 with respect to the neutrophil functions.
研究了浓度为10^(-8) - 10^(-2) mol/l的H2O2对中性粒细胞产生活性氧和氯物质（ROCS）以及分泌髓过氧化物酶（MPO）能力的影响，并且在本研究中还探究了H2O2对中性粒细胞的损伤作用。结果显示，浓度为2×10^(-3) - 2×10^(-2) mol/l的H2O2会导致中性粒细胞膜屏障特性紊乱以及乳酸脱氢酶释放。在中性粒细胞孵育过程中添加10^(-4) - 10^(-7) mol/l的H2O2会使细胞在吞噬过程中产生活性氧和氯物质的能力增强，而在黏附过程中中性粒细胞向细胞外介质中分泌MPO和活性氧和氯物质的能力降低。H2O2的作用机制与花生四烯酸代谢相关。抑制5-脂氧合酶或环氧化酶的代谢途径会增强H2O2对细胞的破坏作用。抑制5-脂氧合酶途径会消除H2O2对MPO和活性氧和氯物质分泌的影响，并增强H2O2对中性粒细胞在吞噬过程中产生活性氧和氯物质能力的作用。所获得的数据证明中性粒细胞对H2O2的破坏作用具有较高抗性，并证实了H2O2对中性粒细胞功能的调节作用。
