Allen J C, Kelly P C
Infect Immun. 1975 Aug;12(2):318-23. doi: 10.1128/iai.12.2.318-323.1975.
We investigated the effect of FeSO4 on phagocytosis-associated, increased oxidative metabolism via the hexose monophosphate shunt, with special attention to its effect on H2O2 levels. The availability of glutathione peroxidase and glutathione reductase for H2O2 disposal and hexose monophosphate shunt stimulation also are evaluated. The results show an impairment of phagocytosis-associated hexose monophosphate shunt activity together with an increase both of resting and phagocytosing formate oxidation. These apparently paradoxical findings are resolved by demonstrating a direct enhancement of formate oxidation by FeSO4 in a cell-free system. In addition, measurement of H2O2 concentrations via scopoletin fluorescence shows reduction of H2O2 by FeSO4. There is no effect on either glutathione peroxidase or glutathione reductase activities. These data suggest that one mechanism of FeSO4 impairment of microbicidal activity is by its removal of H2O2.
我们研究了硫酸亚铁(FeSO4)对吞噬作用相关的、通过磷酸己糖途径增加的氧化代谢的影响,并特别关注其对过氧化氢(H2O2)水平的影响。同时还评估了谷胱甘肽过氧化物酶和谷胱甘肽还原酶在处理H2O2以及刺激磷酸己糖途径方面的可用性。结果显示,吞噬作用相关的磷酸己糖途径活性受损,同时静息状态和吞噬状态下的甲酸氧化均增加。通过在无细胞系统中证明FeSO4直接增强甲酸氧化,解决了这些明显矛盾的发现。此外,通过 scopoletin 荧光测量H2O2浓度显示FeSO4可使H2O2减少。FeSO4对谷胱甘肽过氧化物酶或谷胱甘肽还原酶的活性均无影响。这些数据表明,FeSO4损害杀菌活性的一种机制是通过去除H2O2。