Abstract
The toxic effects of prolonged exposure to O2 during [human] hyperoxic therapy are separable into an acute or edematous-exudative phase of O2 toxicity and a subacute or chronic proliferative phase. O2 toxicity is manifested by a characteristic pattern of inhibition of lung cell nucleotide and protein synthesis. The O2-free radicals and pulmonary antioxidant enzyme defense systems are discussed. An important feature lacking in the experimental studies of O2 toxicity is an explanation of individual variation in susceptibility/resistance to O2 toxicity.