Modelling cortical cataractogenesis: 3. In vivo effects of vitamin E on cataractogenesis in diabetic rats

Adult rats, some pretreated for 2 weeks with daily injections of vitamin E (961 IU/kg) were made diabetic by an intravenous injection of streptozotocin. The glucose levels in the serum rose to about five times normal in both groups. In the animals that had not been treated with vitamin E, changes appeared in the lenses that worsened as the hyperglycemia continued: by 4 days, irregular structure of the fibre cells at the equator; by 1 week, twisted ends and irregular undulations of these cells; by 2 weeks, jagged protrusions from the cell surfaces and twisting of the entire cell; by 3 weeks, flakiness of the surfaces of the equatorial epithelial cells, and disorganized and jagged fibre cells in a large area at the equator; and by 6 weeks, extensive subcapsular globular degeneration of the cortical fibre cells. In contrast, the lenses of the diabetic animals that continued to receive vitamin E showed minimal changes: after 6 weeks the equatorial fibre cells displayed the structural irregularities found after 4 days in the diabetic control animals. The protective effect of vitamin E could not be ascribed to the effect on aldose reductase, for at 6 weeks the levels of fructose and glucose in the lenses of the diabetic animals treated with the vitamin, although increased, were not significantly different from those in the lenses of the untreated diabetic rats, and the sorbitol levels were significantly higher in the treated animals. These results are discussed in terms of a multistep mechanism of cortical cataractogenesis.