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J. G. Parikh, R. N. Khurana, G.-S. Wu, G. Pararajasegaram, N. A. Rao; Photoreceptor Oxidative Damage and Apoptosis in Sympathetic Ophthalmia. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5136.
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In experimental autoimmune uveoretinitis, oxidative stress-induced lipid peroxidation involving the photoreceptors occurs primarily at the inner segment region, where mitochondria are abundant. In humans, sympathetic ophthalmia (SO) is believed to be an autoimmune process directed at the uveal tyrosinase peptide. Experimental uveitis induced by this peptide reveals histologic features of SO. The purpose of the study is to determine the presence of lipid peroxidation in enucleated human eyes with SO.
Sections from eight enucleated SO globes were immunofluorescently stained with rabbit anti-conjugated acrolein antibody. Controls consisted of (1) sections from the same globes stained with anti-acrolein antibody after absorbing with acrolein (2) without primary antibody (3) iso-type immunoglobin substituted for the primary anti-acrolein antibody and (4) sections from two normal human autopsy globes stained with anti-acrolein antibody. Apoptosis in the retinas of the globes was detected using the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method.
Five of eight SO globes showed intense staining for acrolein in the photoreceptor inner segment. The remaining globes revealed mild staining in the same region. None of the controls demonstrated staining for acrolein. Retinas of SO globes revealed the presence of TUNEL-positive photoreceptor cells and middle nuclear layer cells. The control autopsy globes were negative for acrolein staining and TUNEL-positive cells.
. The results indicate that similar to the exprimental uveitis, in sympathetic ophthalmia, there is selective lipid peroxidation involving the photoreceptor inner segments, likely due to mitochondrial oxidative stress, which is known to lead to apoptosis of photoreceptor cells.
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