Antioxidants and Retinopathy
Superoxide dismutase and retinal damage. A newborn rat model of retinopathy was used to test the hypothesis that a lack of the antioxidant superoxide dismutase (SOD) contributes to retinal damage. The study concluded that delivery of SOD to the retina via long-circulating liposomes was beneficial, and suggested the potential value of restoration or supplementation of antioxidants in retinal tissue as a therapeutic strategy (Niesman 1997). It is difficult to provide SOD directly to the retina, but adequate supplementation with nutrients (eg, zinc, copper, and manganese) provide the minerals needed for the formation of SOD in the cells.
Decreased retinal antioxidant activity in diabetics. Enzymatic activities that protect the retina from reactive oxygen species were investigated in diabetic rats known to have retinopathy. Diabetes significantly decreased the activities of glutathione reductase and glutathione peroxidase in the retina. Activities of two other important antioxidant defense enzymes--superoxide dismutase (SOD) and catalase--were also decreased by >25% in the retinas of diabetic rats (Kowluru 1997).
The study showed that diabetes is associated with significant impairment of the antioxidant defense system and antioxidant supplementation can help alleviate the subnormal activities of antioxidant defense enzymes. Administration of supplemental vitamins C and E for 2 months prevented diabetes-induced impairment of the antioxidant defense system in the retina (Kowluru 1997). Another study found no protective effect from antioxidant nutrients for diabetic retinopathy. Authors concluded that further research is necessary to confirm associations between nutrient antioxidant intake and the disease (Mayer-Davis 1998).