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.
Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery
