...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical and diagnostic laboratory immunology >Hemoglobin Toxicity in Experimental Bacterial Peritonitis Is Due to Production of Reactive Oxygen Species
【24h】

Hemoglobin Toxicity in Experimental Bacterial Peritonitis Is Due to Production of Reactive Oxygen Species

机译：实验性细菌性腹膜炎的血红蛋白毒性是由于活性氧的产生

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hemoglobin (Hb) is a toxic molecule responsible for the extreme lethality associated with experimental Escherichia coliperitonitis, but the mechanism has yet to be elucidated. Hb, but not globin, showed toxic effects in a live E. coli model but not in a model using killed E. coli. Methemoglobin, hematin, and the well-known Fenton reagents iron and iron-EDTA demonstrated the same lethal effect in E. coli peritonitis as Hb, while the addition of the Fenton inhibitors desferrioxamine (DF) and diethylenetriamine pentaacetate removed most of the cytotoxic activity of iron. Administration of a combined dose of superoxide dismutase and catalase minimized the action of Hb and iron-EDTA, suggesting that both O2 ? ? and H2O2 are involved in the toxic action of Hb in this rat model. The combination of the antioxidative enzymes and DF further suppressed iron-mediated lethality. An electron spin resonance technique with the spin-trapping reagent 5,5-dimethyl-1-pyroline-N-oxide (DMPO) showed O2 ? ? generation in the peritoneal fluid of rats injected with E. coli alone or E. coliplus iron-DF, and ?OH generation was detected in the peritoneal fluid of the rats injected with iron-EDTA. Hb did not show any spin adduct of oxygen radicals, suggesting that Hb produces non-spin-trapping radical ferryl ion, which decayed the spin adduct of DMPO. In the presence of Hb or iron-EDTA, O2 ?-generating activity and viability of phagocytes decreased, whereas lipid peroxidation of peritoneal phagocytes increased. Generation of oxygen radicals and lipid peroxidation did not differ in the live and dead bacterial models. Bacterial numbers in the peritoneal cavity and blood were markedly increased in the live bacterial model with Hb and iron-EDTA. The Fenton inhibitor iron-DF prevented the loss of phagocyte function, lipid peroxidation, and bacterial proliferation. These results led us to conclude that the lethal toxicity of Hb in bacterial peritonitis is associated with a Fenton-type reaction, the products of which decrease phagocyte viability, through the induction of lipid peroxidation, allowing bacterial proliferation and resulting in mortality.
机译：血红蛋白（Hb）是一种毒性分子，可导致与实验性大肠杆菌腹膜炎有关的极致致命性，但其机理尚待阐明。血红蛋白在活的大肠杆菌中表现出毒性作用，但没有球蛋白。大肠杆菌模型，但不是在使用杀死的 E的模型中。大肠杆菌。高铁血红蛋白，血红素和著名的Fenton试剂铁和铁-EDTA在 E中显示出相同的致死作用。大肠杆菌腹膜炎为Hb，而加入Fenton抑制剂去铁草胺（DF）和五乙酸二亚乙基三胺消除了铁的大部分细胞毒性。联合施用超氧化物歧化酶和过氧化氢酶可使Hb和铁EDTA的作用最小化，表明O 2 ？ ？和H 2 O 2 参与了Hb在该大鼠模型中的毒性作用。抗氧化酶和DF的组合进一步抑制了铁介导的致死性。用自旋俘获剂5,5-二甲基-1-吡咯啉- N -氧化物（DMPO）进行的电子自旋共振技术显示O 2 ？ E的大鼠腹膜液中sup> ？的产生。大肠杆菌或 E。在注射EDTA铁的大鼠腹膜液中检测到大肠杆菌加铁DF和？ OH。 Hb没有显示出任何氧自由基的自旋加合物，表明Hb产生了非自旋捕获的自由基亚铁离子，从而降低了DMPO的自旋加合物。在Hb或EDTA铁存在下，吞噬细胞的产生O 2 ？的活性和活力降低，而腹膜吞噬细胞的脂质过氧化作用增加。在活细菌模型和死细菌模型中，氧自由基的产生和脂质过氧化作用均无差异。在Hb和EDTA铁的活细菌模型中，腹膜腔和血液中的细菌数量显着增加。 Fenton抑制剂铁-DF可以防止吞噬细胞功能的丧失，脂质过氧化和细菌增殖。这些结果使我们得出结论，Hb对细菌性腹膜炎的致死毒性与Fenton型反应有关，该反应的产物通过诱导脂质过氧化作用降低吞噬细胞的活力，从而使细菌增殖并导致死亡。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号