Abstract
Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules.
Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide.
Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.
Keywords: Oxidative stress, oxidative damage, ocular diseases, keratoconus, cataract, retinopathy.
Current Pharmaceutical Design
Title:Oxidative Stress, Ocular Disease and Diabetes Retinopathy
Volume: 24 Issue: 40
Author(s): Orathai Tangvarasittichai and Surapon Tangvarasittichai*
Affiliation:
- Chronic Diseases Research Unit, Department of Medical Technology, Faculty of Allied Health Sciences, Naresuan University, 99 Moo 9 Tambon Tha Pho, Muang Phitsanulok 65000,Thailand
Keywords: Oxidative stress, oxidative damage, ocular diseases, keratoconus, cataract, retinopathy.
Abstract: Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules.
Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide.
Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.
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Cite this article as:
Tangvarasittichai Orathai and Tangvarasittichai Surapon *, Oxidative Stress, Ocular Disease and Diabetes Retinopathy, Current Pharmaceutical Design 2018; 24 (40) . https://dx.doi.org/10.2174/1381612825666190115121531
DOI https://dx.doi.org/10.2174/1381612825666190115121531 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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