Photoreceptor Oxidative Damage in ympathetic Ophthalmia Original Reearch Article

Purpoe To determine photoreceptor oxidative tre and damage in ympathetic ophthalmia (O). Deign Immunohitologic tudy. Method Eight formalin-fixed and paraffin-embedded human globe with typical hitologic feature of O and five age-matched globe without intraocular inflammation (control) were retrieved from the Doheny Eye Intitute ophthalmic pathology file. Deparaffinized ection of the globe were proceed to localize tumor necroi factor-α (TNF-α), tumor necroi factor receptor-1 (TNF-R1), acrolein, inducible nitric oxide ynthae (iNO), and nitrotyroine by immunolocalization method. The latter two were localized to photoreceptor mitochondria uing anti–cytochrome C antibody. Apoptotic cell were detected by Terminal deoxynucleotidyl tranferae biotin-dUTP Nick End Labeling (TUNEL) aay and were localized to the ite of oxidative tre uing antinitrotyroine antibody. Reult Increaed expreion of TNF-α can be een in the photoreceptor nuclear layer in all O globe, wherea no uch expreion wa oberved in control globe. TNF-R1, iNO, acrolein, and nitrotyroine were immunolocalized to the inner egment of the photoreceptor in all O globe, but only mild focal taining wa oberved in the control retina. Both nitrotyroine and iNO immunolocalization revealed poitive taining retricted primarily to mitochondria at the inner egment of the photoreceptor. Mot of the TUNEL-poitive cell were detected in the photoreceptor at the ite of nitrotyroine taining. In contrat, the age-matched control globe howed negative reult. Concluion In O, photoreceptor mitochondrial oxidative tre occur in the abence of leukocytic infiltration of the retina and may lead to photoreceptor apoptoi and ubequent viion lo. The oxidative tre eem to be mediated by iNO and TNF-α. The current anti-inflammatory therapy combined with agent that could prevent oxidative tre may prevent photoreceptor damage in O and may preerve viion.