Photoreceptor mitochondrial oxidative stress in experimental autoimmune uveitis.

In experimental autoimmune uveitis (EAU), the macrophages infiltrate the retina during the late phase, 10-14 days after immunization with uveitogenic antigen, causing photoreceptor damage. However, prior to inflammatory cell infiltration, during the early phase (5-7 days after immunization), increased generation of reactive oxygen and nitric oxide species was observed in the photoreceptor mitochondria indicating oxidative stress. The oxidative-stress-induced nitration of photoreceptor mitochondrial proteins and peroxidation of membrane lipids led to activation and migration of microglia toward the photoreceptors. These observations suggest oxidative stress could be an initial pathologic event leading to amplification of inflammation inducing photoreceptor damage, thereby causing clinical and histologic expression of uveitis in the form of inflammatory cell infiltration.