Mikoian V D, Kubrina L N, Vanin A F
Biokhimiia. 1996 Jul;61(7):1182-8.
Coinjection of citrate iron complex (7.5-10 mg iron/kg) with Escherichia coli lipopolysaccharide (LPS) inhibited generation of nitric oxide in the liver of mice caused by LPS-dependent synthesis of inducible NO-synthase (iNOS). Coinjection of hydroquinone, pyrogallol, or CCl4 with LPS also inhibited NO generation in the liver. Inhibition of LPS-dependent of NO synthesis in the liver by all these agents and iron can be due to their pro-oxidant effects on metabolism of this tissue. These pro-oxidants rapidly activate synthesis of low molecular weight antioxidants; LPS-dependently generated active oxygen forms in the liver of treated animals, which causes iNOS synthesis, are inactivated by the antioxidants; thus, accumulation of active oxygen species is decreased and iNOS synthesis is inhibited.
将柠檬酸铁复合物(7.5 - 10毫克铁/千克)与大肠杆菌脂多糖(LPS)共同注射,可抑制LPS依赖性诱导型一氧化氮合酶(iNOS)合成所导致的小鼠肝脏中一氧化氮的生成。将对苯二酚、邻苯三酚或四氯化碳与LPS共同注射,也可抑制肝脏中一氧化氮的生成。所有这些试剂和铁对肝脏中LPS依赖性一氧化氮合成的抑制作用,可能归因于它们对该组织代谢的促氧化作用。这些促氧化剂可迅速激活低分子量抗氧化剂的合成;经处理动物肝脏中LPS依赖性产生的活性氧形式(其可导致iNOS合成)会被抗氧化剂灭活;因此,活性氧物种的积累减少,iNOS合成受到抑制。