ABNORMALITIES OF RETINAL METABOLISM IN DIABETES OR GALACTOSEMIA - ATPASES AND GLUTATHIONE

Purpose. Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear. Defects of retinal metabolism th at are common to galactosemia and diabetes are closely associated with the development of retinopathy and might play a role in the pathogene sis of the retinal disease. Methods. Effects of experimental galactose mia on retinal calcium-activated ATPase [(Ca,Mg)-ATPase], sodium-potas sium ATPase [(Na,K)-ATPase], glutathione, ATP, and pertinent ions have been compared with the effects of experimental diabetes in rat and do g models of diabetic retinopathy. Results. Activities of (Ca,Mg)-ATPas e and (Na,K)-ATPase were decreased as a result of either experimental galactosemia or diabetes in both the dog and the rat, and the decrease s were accompanied by a diminution of reduced glutathione (GSH) in the retina. Ouabain-insensitive ATPase activity in the retina was not sig nificantly reduced by diabetes or galactosemia, suggesting that the ob served defects in (Ca,Mg)-ATPase and (Na,K)-ATPase activities were spe cific. The decrease of retinal GSH level was associated with an elevat ed concentration of oxidized glutathione in diabetes but not in galact osemia. Retinal ATP and ion concentrations remained unaffected by expe rimental galactosemia or diabetes. Conclusions. Comparison of two etio logically dissimilar models of diabetic retinopathy (diabetes and gala ctosemia) has revealed abnormalities of retinal metabolism that are sh ared by the two models. Further comparisons of retinal metabolism betw een these two models should reveal additional sequelae of hyperglycemi a that are associated with, and that might play a role in, the develop ment of diabetic retinopathy.