Abstract
Light-induced oxidation of lipids and proteins provokes retinal injuries and results in progression of degenerative retinal diseases, such as, for instance, iatrogenic photic maculopathies. Having accumulated over years retinal injuries contribute to development of age-related macular degeneration (AMD). Antioxidant treatment is regarded as a promising approach to protecting the retina from light damage and AMD. Here, we examine oxidative processes induced in rabbit retina by excessive light illumination with or without premedication using mitochondria-targeted antioxidant SkQ1 (10-(6’-plastoquinonyl)decyltriphenyl-phosphonium). The retinal extracts obtained from animals euthanized within 1–7 days post exposure were analyzed for H2O2, malondialdehyde (MDA), total antioxidant activity (AOA), and activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) using colorimetric and luminescence assays. Oxidation of visual arrestin was monitored by immunoblotting. The light exposure induced lipid peroxidation and H2O2 accumulation in the retinal cells. Unexpectedly, it prominently upregulated AOA in retinal extracts although SOD and GPx activities were compromised. These alterations were accompanied by accumulation of disulfide dimers of arrestin revealing oxidative stress in the photoreceptors. Premedication of the eyes with SkQ1 accelerated normalization of H2O2 levels and redox-status of lipids and proteins, contemporarily enhancing AOA and, likely, sustaining normal activity of GPx. Thus, SkQ1 protects the retina from light-induced oxidative stress and could be employed to suppress oxidative damage of proteins and lipids contributing to AMD.
Highlights
The mammalian retina is highly vulnerable to oxidative stress
We demonstrated that the illumination enhances lipid peroxidation and hydrogen peroxide levels in the retinal cells, which is associated with decrease in activity of antioxidant defense enzymes, superoxide dismutase (SOD), and glutathione peroxidase (GPx)
Light-induced oxidative damage in the retina was simulated in the following animal model
Summary
The mammalian retina is highly vulnerable to oxidative stress. photoreceptor and retinal pigment epithelium (RPE) cells generate high levels of reactive oxygen species (ROS) due to a number of factors. Photoreceptors are constantly exposed to light and contain a number of different photosensitizer molecules They metabolize and function under high oxygen. The recycling of photoreceptor discs suffering from oxidative damage is performed via their phagocytosis by RPE and oxidative damage to photoreceptors induces intense accumulation of ROS in pigment epithelium [3]. These processes impose a great risk on the retina, especially in older people, as retinal neurons and RPE cells become especially susceptible to oxidative damage in the aging tissue [4,5]
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