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Photoreceptor oxidative damage in sympathetic ophthalmia.

Abstract：

PURPOSE:To determine photoreceptor oxidative stress and damage in sympathetic ophthalmia (SO). DESIGN:Immunohistologic study. METHODS:Eight formalin-fixed and paraffin-embedded human globes with typical histologic features of SO and five age-matched globes without intraocular inflammation (controls) were retrieved from the Doheny Eye Institute ophthalmic pathology files. Deparaffinized sections of the globes were processed to localize tumor necrosis factor-alpha (TNF-alpha), tumor necrosis factor receptor-1 (TNF-R1), acrolein, inducible nitric oxide synthase (iNOS), and nitrotyrosine by immunolocalization method. The latter two were localized to photoreceptor mitochondria using anti-cytochrome C antibody. Apoptotic cells were detected by Terminal deoxynucleotidyl transferase biotin-dUTP Nick End Labeling (TUNEL) assay and were localized to the site of oxidative stress using antinitrotyrosine antibody. RESULTS:Increased expression of TNF-alpha can be seen in the photoreceptor nuclear layer in all SO globes, whereas no such expression was observed in control globes. TNF-R1, iNOS, acrolein, and nitrotyrosine were immunolocalized to the inner segments of the photoreceptors in all SO globes, but only mild focal staining was observed in the control retinas. Both nitrotyrosine and iNOS immunolocalization revealed positive staining restricted primarily to mitochondria at the inner segments of the photoreceptors. Most of the TUNEL-positive cells were detected in the photoreceptors at the site of nitrotyrosine staining. In contrast, the age-matched control globes showed negative results. CONCLUSIONS:In SO, photoreceptor mitochondrial oxidative stress occurs in the absence of leukocytic infiltration of the retina and may lead to photoreceptor apoptosis and subsequent vision loss. The oxidative stress seems to be mediated by iNOS and TNF-alpha. The current anti-inflammatory therapy combined with agents that could prevent oxidative stress may prevent photoreceptor damage in SO and may preserve vision.

journal_name

Am J Ophthalmol

journal_title

American journal of ophthalmology

authors

Parikh JG,Saraswathy S,Rao NA

doi

10.1016/j.ajo.2008.03.026

subject

Has Abstract

pub_date

2008-12-01 00:00:00

pages

866-75.e2

issue

6

eissn

0002-9394

issn

1879-1891

pii

S0002-9394(08)00257-2

journal_volume

146

pub_type

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