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Diabetic retinopathy is the leading cause of blindness among the working population.
Although other mechanisms may play a role, there are several lines of evidence that have implicated increased activity of intracellular enzyme aldose reductase as a major mechanism for pathological changes in both galactosemic and diabetic retinopathy. We have already established that sustained ARI delivery in the eye using biodegradable drug delivery devices is effective at suppressing sorbitol accumulation in the retina of transgenic diabetic rats in spite of the continuous hyperglycemic state of these rats. We have also discovered that VEGF levels are up-regulated in the retina of diabetic animal eyes very early in the development of diabetic retinopathy. We now want to determine whether the total inhibition of intracellular galactitol accumulation in the retina by sustained local delivery of a potent aldose reductase inhibitor will block the mechanisms leading to the breakdown of the blood-retina barrier in hypergalactosemic animals. We also want to establish that inhibition of retinal galactitol accumulation will decrease the retinal VEGF levels in hypergalactosemic animals.