It HAS long been known that no living matter is exempt from the deleterious effects of increased oxygen tensions. Both in man and experimental animals pulmonary and central nervous system symptoms and pathology have been repeatedly observed following administration of high concentrations of oxygen (I). Under ordinary clinical conditions the concentration of therapeutically administered oxygen is not great enough and/or administration is not prolonged enough to give rise to recognizable pathology. Since the oxygen therapy given to premature infants is often intensive and prolonged and since the incidence of retrolental fibroplasia (RLF) seems to have increased sharply since oxygen therapy has been in general use in premature nurseries, it occurred to many investigators that the use of oxygen might somehow play a part in th e development of the disease. Reports from several clinics stated that the incidence of retrolental fibroplasia sharply declined following the abandonment of oxygen therapy (2-5). It has also been noted that some factors increasing metabolism increase vulnerability to oxygen poisoning (I, 6). Warburg and others (7, 8) have shown that retina has a higher rate of respiration and of anaerobic glycolysis than any other tissue studied by them. From studies with retinas of chick embryos (Krebs and Kiyohara cit. in 9) there is also an indication that oxygen consumption in them is even higher than in adult retinas. From the above considerations it is conceivable that immature retinas might be highly sensitive to oxygen poisoning. It has also been suggested that changes observed in the eyes of young vitamin E-deficient