Autoxidative damage to the retina: potential role in retinopathy of prematurity

Abstract

Oxygen can participate in a number of reactions that are potentially damaging to cells and tissues. Reactive forms of oxygen are generated during normal metabolic processes, and a variety of biologic mechanisms have evolved to protect organisms from damage by these compounds. Apparently these protective mechanisms are not fully developed in the fetus, which exists in a hypoxic environment in utero. Premature birth exposes the infant to a sudden increase in environmental oxygen content, for which it is not physiologically prepared. It is likely that this premature exposure to atmospheric oxygen triggers an elevation in the rate of autoxidative reactions in tissues and that the termination of normal retinal vascularization seen in ROP is the result of an attempt to minimize such reactions. This interpretation is supported by the finding that vitamin E, an antioxidant in vivo, reduces the severity of ROP when given at an early enough stage.