Victor Victor M, Rocha Milagros, De la Fuente Monica
Unidad Mixta Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III-Universidad de Valencia, Avda. Blasco Ibañez 15, 46010 Valencia, Spain.
Int Immunopharmacol. 2004 Mar;4(3):327-47. doi: 10.1016/j.intimp.2004.01.020.
The excessive production of reactive oxygen species (ROS), associated with inflammation, leads to a condition of oxidative stress. Oxidative stress is a major contributing factor to the high mortality rates associated with several diseases such as endotoxic shock. This condition can be controlled to a certain degree by antioxidant therapies. Immune cells use ROS in order to support their functions and therefore need adequate levels of antioxidant defenses in order to avoid the harmful effect of an excessive production of ROS. This review discusses the toxic effects of endotoxin, paying particular attention to immune function. It continues by analyzing the mechanism to which specific cells of the immune system recognize endotoxin, and the resulting pathways leading to nuclear factor-kappaB activation and proinflammatory gene transcription. We also focus on the involvement of reactive oxygen and nitric oxide (NO) and the protective role of antioxidants. The potential clinical use of antioxidants in the treatment of sepsis and the effects on the redox state of the immune cells are discussed.
与炎症相关的活性氧(ROS)过度产生会导致氧化应激状态。氧化应激是导致诸如内毒素休克等多种疾病高死亡率的主要因素。这种情况可以通过抗氧化疗法在一定程度上得到控制。免疫细胞利用ROS来支持其功能,因此需要足够水平的抗氧化防御以避免ROS过度产生的有害影响。本综述讨论了内毒素的毒性作用,特别关注免疫功能。接着分析了免疫系统特定细胞识别内毒素的机制,以及导致核因子-κB激活和促炎基因转录的途径。我们还关注活性氧和一氧化氮(NO)的作用以及抗氧化剂的保护作用。讨论了抗氧化剂在脓毒症治疗中的潜在临床应用及其对免疫细胞氧化还原状态的影响。