Cytochrome Oxidase Activity in the Fetal Sheep Retina
Oxidative metabolism in the retina is dependent upon mitochondrial cytochrome c oxidase (COX), which is the terminal enzyme in the respiratory chain. Because of its powerful reducing capacity, COX functions as critical antioxidant thereby protecting cell membranes from peroxidative free radical damage by superoxide, hydrogen peroxide, hydroxyl radical as well as other oxygen species. COX is most abundant in the retinal pigment epithelium (RPE) but there is also high COX activity ijn the photoreceptor inner segments and lesser activity in the synaptic and ganglion cell layers (1). COX is present in the fetal sheep retina by 120 days gestational age (2; term = 148d). However, the subunit composition, kinetics and activity of fetal COX, as compared to the adult, have not been studied previously (3). This pilot study was undertaken to elucidate some of the potential mechanisms of the retinal pathobiology seen in very low birth weight, premature infants (<1000gm) who are necessarily exposed to an increased PIO2 resulting from air breathing. In about 27% of these infants, the ensuing “Retinopathy of Prematurity” causes varying degrees of visual impairment totaling about 5000 cases per year in the U.S. (4).
KeywordsHydrogen Peroxide Hydroxyl Superoxide Retina
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