Although oxygen has been known to be toxic for more than 200 years, the clinical importance of oxygen toxicity was not appreciated until an epidemic of retrolental fibroplasia occurred in the early 1950s. Oxygen at high partial pressures is toxic to the respiratory, cardiovascular, nervous, and gastrointestinal systems. Toxicity results from the formation of oxygen-free radicals. These arise within mitochondria as oxygen is reduced to water, as byproducts of prostaglandin and thromboxane synthesis, and by the xanthine oxidase catalyzed reduction of xanthine or hypoxanthine. They are also produced by activated macrophages as part of the immune response. Superoxide anion is the radical most commonly produced. It dismutes to hydrogen peroxide, which is able to diffuse through lipid membranes. Hydrogen peroxide reacts with transition metals to produce the highly reactive hydroxyl radical which can initiate chain reactions of lipid peroxidation leading to cell rupture. Oxygen radical scavengers such as superoxide dismutase and catalase protect the body against normal levels of oxygen-free radicals. Oxygen toxicity can result from either reperfusion of ischemic tissue or prolonged exposure to high concentrations of oxygen. Limiting hyperoxia to maintain arterial oxygen percent saturation (SaO2) greater than or equal to 90% is recommended.
尽管人们知道氧气具有毒性已有200多年，但直到20世纪50年代初发生了晶状体后纤维增生症的流行，氧气毒性的临床重要性才得到重视。高分压的氧气对呼吸、心血管、神经和胃肠系统有毒性。毒性是由氧自由基的形成引起的。这些自由基在线粒体内随着氧气被还原成水而产生，是前列腺素和血栓素合成的副产物，并且由黄嘌呤氧化酶催化黄嘌呤或次黄嘌呤的还原产生。它们也作为免疫反应的一部分由活化的巨噬细胞产生。超氧阴离子是最常产生的自由基。它歧化成过氧化氢，而过氧化氢能够扩散穿过脂质膜。过氧化氢与过渡金属反应产生高活性的羟基自由基，后者可引发脂质过氧化的连锁反应，导致细胞破裂。超氧化物歧化酶和过氧化氢酶等氧自由基清除剂可保护身体免受正常水平的氧自由基侵害。氧气毒性可由缺血组织的再灌注或长时间暴露于高浓度氧气引起。建议将高氧血症限制在动脉血氧饱和度（SaO2）大于或等于90%。
