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Mitochondria‐derived Reactive Oxygen Species Mediate Blue Light‐induced Death of Retinal Pigment Epithelial Cells ¶
Author(s) -
King Ayala,
Gottlieb Eyal,
Brooks David G.,
Murphy Michael P.,
Dunaief Joshua L.
Publication year - 2004
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2004.tb00036.x
Subject(s) - mitochondrion , reactive oxygen species , programmed cell death , oxidative stress , retinal pigment epithelium , microbiology and biotechnology , retinal , retina , biology , macular degeneration , apoptosis , chemistry , biophysics , biochemistry , medicine , ophthalmology , neuroscience
Throughout the lifetime of an individual, light is focused onto the retina. The resulting photooxidative stress can cause acute or chronic retinal damage. The pathogenesis of age‐related macular degeneration (AMD), the leading cause of legal blindness in the developed world, involves oxidative stress and death of the retinal pigment epithelium (RPE) followed by death of the overlying photoreceptors. Evidence suggests that damage due to exposure to light plays a role in AMD and other age‐related eye diseases. In this work a system for lightinduced damage and death of the RPE, based on the human ARPE‐19 cell line, was used. Induction of mitochondriaderived reactive oxygen species (ROS) is shown to play a critical role in the death of cells exposed to short‐wavelength blue light (425 ± 20 nm). ROS and cell death are blocked either by inhibiting the mitochondrial electron transport chain or by mitochondria‐specific antioxidants. These results show that mitochondria are an important source of toxic oxygen radicals in blue light‐exposed RPE cells and may indicate new approaches for treating AMD using mitochondria‐targeted antioxidants.