Jenkinson S G
Division of Pulmonary Diseases/Critical Care Medicine, University of Texas Health Science Center, San Antonio.
Clin Chest Med. 1989 Mar;10(1):37-47.
Exposure to hyperoxia or a number of different environmental toxins can result in free radical-mediated lung injury. Specific toxins and their activated breakdown products can produce free radicals and markedly change normal lung metabolism by reacting with cell membranes, intracellular proteins, and nucleic acids. Endogenous production of free radicals by polymorphonuclear leukocytes sequestered in the lung can also lead to lung damage. Numerous intracellular and extracellular free radical defenses are present in human lung to detoxify these oxygen species as they are being formed. Lung injury will begin to occur if free radical production overcomes lung antioxidant defenses.
暴露于高氧环境或多种不同的环境毒素可导致自由基介导的肺损伤。特定毒素及其活化分解产物可产生自由基,并通过与细胞膜、细胞内蛋白质和核酸反应,显著改变正常的肺代谢。聚集在肺内的多形核白细胞内源性产生自由基也可导致肺损伤。人类肺组织中存在大量细胞内和细胞外自由基防御机制,以便在这些氧物种形成时将其解毒。如果自由基产生超过肺抗氧化防御能力,肺损伤将开始发生。