Housset B
Presse Med. 1984 Oct 20;13(37):2257-60.
Prolonged breathing of normobaric oxygen can be responsible for pulmonary lesions which are frequently fatal. It is highly probable that this toxicity largely results from excessive production, by the alveolar cells, of free radicals derived from oxygen. The lung contains a number of enzymatic systems (superoxide dismutase, catalase, glutathione peroxidase) or non-enzymatic systems (vitamins C and E, glutathione) capable of preventing lesions induced by these radicals. However, the respective role of the various anti-oxidants in this tolerance to oxygen remains uncertain. Numerous aspects of pulmonary oxygen toxicity are still poorly understood, but in vivo and in vitro studies, now being vigorously pursued, show promises of forthcoming progress in the pathophysiology and treatment of pulmonary oxygen toxicity.
常压氧的长时间吸入可导致肺部病变，这些病变往往是致命的。这种毒性很可能主要是由肺泡细胞过度产生源自氧的自由基所致。肺含有一些酶系统（超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶）或非酶系统（维生素C和E、谷胱甘肽），能够预防这些自由基诱导的损伤。然而，各种抗氧化剂在这种对氧的耐受性中的各自作用仍不确定。肺部氧中毒的许多方面仍知之甚少，但目前正在大力开展的体内和体外研究显示，在肺部氧中毒的病理生理学和治疗方面即将取得进展。
