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首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Neutrophil-endothelial cell interaction. Evidence for and mechanisms of the self-protection of bovine microvascular endothelial cells from hydrogen peroxide-induced oxidative stress.
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Neutrophil-endothelial cell interaction. Evidence for and mechanisms of the self-protection of bovine microvascular endothelial cells from hydrogen peroxide-induced oxidative stress.

机译：中性粒细胞-内皮细胞相互作用。牛微血管内皮细胞免受过氧化氢诱导的氧化应激自我保护的证据和机制。

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Bovine microvascular endothelial cells (MEC) were able to degrade the H2O2 generated by phorbol myristate acetate-activated bovine neutrophils or by glucose oxidase with a maximal capacity of 4.0 +/- 1.2 (SD) nmol/10(6) cells/min, corresponding to the H2O2 released by about 3 X 10(6) neutrophils. H2O2 degradation occurred via the glutathione redox cycle and catalase. Degradation via the glutathione redox cycle was coupled with a marked stimulation of the hexose monophosphate shunt activity. The effect of H2O2 on ethidium bromide exclusion and on succinate oxidation was studied. Neither parameter was altered when MEC were exposed to H2O2 produced at rates within their degradative capacity. As soon as this was exceeded, impairment of both functions occurred. It is concluded that endothelial cells can protect themselves from H2O2-induced injury in a well-defined range of environmental H2O2 concentrations by actively degrading the peroxide.
机译：牛微血管内皮细胞（MEC）能够降解佛波醇肉豆蔻酸酯乙酸盐激活的牛嗜中性粒细胞或葡萄糖氧化酶产生的H2O2，最大容量为4.0 +/- 1.2（SD）nmol / 10（6）细胞/分钟，对应约3 X 10（6）中性粒细胞释放出H2O2。 H2O2降解通过谷胱甘肽氧化还原循环和过氧化氢酶发生。通过谷胱甘肽氧化还原循环的降解与己糖单磷酸酯旁路活性的明显刺激相结合。研究了过氧化氢对溴化乙锭排阻和琥珀酸氧化的影响。当MEC暴露于降解能力范围内的H2O2中时，这两个参数都没有改变。一旦超过此限制，就会发生两种功能的损害。结论是，内皮细胞可以通过积极降解过氧化物在一定范围的环境H2O2浓度范围内保护自己免受H2O2诱导的伤害。

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