Superoxide Dismutase (SOD) is an endogenous antioxidant enzyme that catalyzes the conversion of superoxide radicals into hydrogen peroxide and oxygen, thereby reducing oxidative stress. Oxidative stress plays a pivotal role in the pathogenesis of diabetic retinopathy (DR), a diabetes complication characterized by damage to the retinal blood vessels. Experimental studies have shown that retinal tissues in diabetic animals exhibit decreased SOD activity and increased oxidative damage. Supplementation with SOD, or agents that enhance endogenous SOD activity, has demonstrated protective effects against retinal oxidative injury in animal models of diabetes.

However, direct clinical evidence in humans is limited. Some small clinical studies and pilot trials have reported that antioxidant supplementation (including SOD or SOD mimetics) may reduce markers of oxidative stress and slow the progression of early diabetic retinopathy, but these studies are generally preliminary and not sufficiently powered to draw firm conclusions. SOD itself is a large protein and is poorly absorbed orally in its native form, though some formulations (e.g., enteric-coated or plant-extracted SOD) claim improved bioavailability. Overall, while mechanistic and preclinical data support a rationale for SOD in DR, robust clinical validation is lacking.

In summary, SOD is used to support diabetic retinopathy based on scientific understanding of disease mechanisms and positive animal data, but human evidence is preliminary. The level of evidence is rated as 2/5.