Perturbed Biochemical Pathways and Associated Oxidative Stress Lead to Vascular Dysfunctions in Diabetic Retinopathy

Table 1

Oxidants elevated in diabetic retinopathy.

Oxidants	Involvement in DR
Superoxide radicals	Accumulation in retinal cell mitochondria leads to mutations in the mtDNA and induces a phenomenon of “metabolic memory” [132, 133].
Hydroxy radicals	Generated by Fenton reaction and responsible for damage to retinal cells membrane and mtDNA as well as reduction of thinning of outer and inner nuclear layers of the retina [133–135].
Peroxyl radical/lipid peroxides	Lipid peroxidation chain reaction damages retinal cell membrane and creates a redox milieu, as evident by an increase in the vitreous of PDR patients [136, 137].
Hydrogen peroxide	Toxic radical species are increased in retinal cells, and treatment with obestatin prevents the H2O2-induced (retinal ganglion cells) RGC damage [133, 138].
Singlet oxygen	Excitation of oxygen through sunlight and radiation and higher oxygen consumption by retinal cells adds to the impaired redox status of the cell in DR [131].
Peroxynitrite	The reactive nitrogen species shifts the redox status of the cell towards destruction causing apoptosis of retinal endothelial cells [139].