Dobrina A, Patriarca P
J Clin Invest. 1986 Aug;78(2):462-71. doi: 10.1172/JCI112598.
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.
牛微血管内皮细胞（MEC）能够降解由佛波酯肉豆蔻酸酯激活的牛中性粒细胞或葡萄糖氧化酶产生的过氧化氢，最大降解能力为4.0±1.2（标准差）nmol/10⁶细胞/分钟，这相当于约3×10⁶个中性粒细胞释放的过氧化氢量。过氧化氢的降解通过谷胱甘肽氧化还原循环和过氧化氢酶进行。通过谷胱甘肽氧化还原循环的降解与己糖磷酸支路活性的显著刺激相关联。研究了过氧化氢对溴化乙锭排斥和琥珀酸氧化的影响。当MEC暴露于以其降解能力范围内的速率产生的过氧化氢时，这两个参数均未改变。一旦超过这个范围，这两种功能就会受损。得出的结论是，内皮细胞可以通过主动降解过氧化物，在明确的环境过氧化氢浓度范围内保护自身免受过氧化氢诱导的损伤。
