[Pulmonary toxicity of oxygen].
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.
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004361:Drug Tolerance; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D008171:Lung Diseases / Q000201:enzymology / Q000209:etiology / Q000473:pathology; D009747:Nutritional Physiological Phenomena; D010084:Oxidation-Reduction; D010100:Oxygen / Q000009:adverse effects / Q000633:toxicity*; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D005609:Free Radicals; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D010100:Oxygen
Toxicité pulmonaire de l'oxygène.