Authors: Wu, Guey Shuang; Rao, Narsing A

Source: Expert Review of Ophthalmology, Volume 3, Number 3, June 2008 , pp. 299-310(12)

Publisher: Expert Reviews

Abstract:

The complex human intraocular inflammation, uveitis, is the leading cause of blindness in industrialized countries. Experimental autoimmne uveoretinitis (EAU), which mimics the clinical features of the human disease, is characterized by inflammation of the retina and choroid with associated damage, mainly in the outer retina. In EAU, the photoreceptor cell alteration appears early in the disease process, irrespective of the presence of macrophages and other inflammatory cells. These modifications probably derive from cytokine-mediated reactive oxygen and nitrogen species generated within the retina. Mitochondria are copious producers of intracellular reactive oxygen species and reactive nitrogen species. This review discusses the mitochondria-originated photoreceptor cell damage in EAU from the context of peroxynitrite generation, membrane permeability transition pore, cytochrome c release, and protection by Mn superoxide dismutase. Understanding of these processes could possibly lead to the design of therapeutic intervention with a desirable outcome.

Keywords: cytochrome c release; experimental autoimmune uveoretinitis; mitochondria; mitochondrial membrane permeability transition por; nitric oxide synthase; oxidative stress; peroxynitrite; photoreceptor cell; protein tyrosine nitration; reactive nitrogen species; reactive oxygen species

Document Type: Research article

DOI: http://dx.doi.org/10.1586/17469899.3.3.299

Affiliations: 1: Investigator in Doheny Eye Institute, Doheny Eye Institute, University of Southern California, Keck School of Medicine, 1450 San Pablo Street, Los Angeles, CA 90033-1088 USA., Email: nrao@usc.edu

Publication date: 2008-06-01

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