The current hypothesis for the damage caused to mammalian tissues by hyperoxia is that oxygen radicals and related reactive oxygen metabolites are formed at rates which exceed the ability of the cells' natural antioxidant defense mechanisms to detoxify these deleterious products. In this review a very brief description of oxygen pathology is given together with data on the relevance of in vivo tissue pO2 levels. After a short historical account of the biochemistry of oxygen toxicity in the pre-radical days. the evidence for the current status of the radical theory is reviewed. This covers the probable sources of excess reactive oxygen metabolite generation under conditions of increased oxygen tension, and the measurement of the reactive species thought to be important in causing this damage. The large volume of circumstantial evidence, including the production of tolerance, raising or lowering antioxidant defenses and the administration of exogenously produced radicals is considered.