title: Oxygen-induced retinopathy in the rat. Vitamins C and E as potential therapies.
abstract: Oxygen-induced retinopathy (OIR) was produced by subjecting newborn albino rats to a 60% oxygen atmosphere for 14 days before they were killed and retinal analysis was done. The extent of OIR was measured by estimating the severity of retinal vasoobliteration in ink-perfused flat-mounted retinas. This was done with the aid of a digitizing camera and an image-analysis system designed to create binary images of the retinal blood vessels. Retinal levels of several antioxidant molecules also were measured. Alpha-tocopherol and ascorbic acid were reduced in oxygen-exposed rats by 34% and 20%, respectively, compared with room air-raised control animals. Retinal glutathione reductase, S-transferase, and peroxidase showed no differences between oxygen-treated and -untreated rats. Attempts to increase the newborn rats' retinal ascorbic acid by administering daily subcutaneous injections (5 g/kg body weight) to the mother rats were unsuccessful. However, the level of retinal alpha-tocopherol of newborn rats could be altered by dietary manipulation of the mothers. The mothers were fed diets containing either 1 g alpha-tocopherol acetate/kg food or none, starting 21-25 days before the birth of their litters and lasting throughout the exposure period. This treatment resulted in three- to fourfold differences in the retinal alpha-tocopherol levels of the pups. The combination of dietary and oxygen treatments also resulted in significant differences in retinal glutathione peroxidase activity, with the vitamin E-deprived, oxygen-exposed group having highest levels. Newborn rats both supplemented with and deprived of alpha-tocopherol had less vasoobliteration than did those nursed by mothers fed rat chow.
authors.affiliation: Arkansas Center for Eye Research, Little Rock 72205.
authors.forename: J S
authors.initials: JS
authors.lastname: Penn
authors.forename: L A
authors.initials: LA
authors.lastname: Thum
authors.forename: M I
authors.initials: MI
authors.lastname: Naash
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001205:Ascorbic Acid / Q000627:therapeutic use*; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D010100:Oxygen / Q000633:toxicity; D051381:Rats; D011919:Rats, Inbred Strains; D012171:Retinal Vessels / Q000201:enzymology / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000201:enzymology / Q000473:pathology / Q000628:therapy*; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D014810:Vitamin E; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D001205:Ascorbic Acid; D010100:Oxygen