Diabetic retinopathy is the leading cause of blindness and visual disability in the industrialized world. The mechanisms of how diabetic retinopathy develops are still an open question. Alterations contributing to oxidative and nitrosative stress, including elevated nitric oxide (NO) and superoxide production, overexpression of different isoforms of nitric oxide synthase (NOS), nitrated and poly(ADP-ribosy)lated proteins, and downregulation of antioxidative enzymes have been implicated in the pathogenesis of this ocular disease. The possible roles of these components in the development of diabetic retinopathy are reviewed here, and their values as therapeutic targets for inhibiting or delaying the development of diabetic retinopathy are highlighted.