Oxidative Stress: Implications for the Development of Diabetic Retinopathy and Antioxidant Therapeutic Perspectives

Table 1

Antioxidants used in the treatment of DR and their mechanisms of action.

Antioxidants	Mechanisms	References
Vitamins C and E	Free radical scavenging; prevented the inhibition of retinal glutathione reductase, glutathione peroxidase (GPx), and SOD activities	[66, 81, 83]
Vitamin E	Radical scavenger, against lipid peroxidation	[67]
Ascorbic acid, acetate,	Decreased retinal oxidative stress, protein kinase C activity, and nitric oxides; decreased retinal cell loss	[66, 82, 84]
and -tocopherol
beta-Carotene	High tendency to oxidize; decreased retinal oxidative stress, protein kinase C activity, and nitric oxides; decreased retinal cell loss	[66, 83]
alpha-Lipoic acid	Inhibited activation of NF-κB and cell apoptosis; decreased retinal oxidative stress; prevented the reduction of GSH and GPx levels; reduced malondialdehyde (MDA) levels; decreased expression of angiogenic factors	[68–71, 82]
N-Acetylcysteine (NAC)	Inhibition activation of NF-B and cell apoptosis; decreased ROS. VEGF and ICAM-1 expression; inhibited activation of macrophage/microglia; inhibition of perivascular cell changes	[68, 72, 73]
Aminoguanidine	Prevented elevation of retinal oxidative stress, NO, and PKC activity; inhibited lipid peroxidation and AGEs formation	[74, 75]
Curcumin	Multipotent activities prevent the decrease in the antioxidant capacity and increase in oxidative stress; inhibit diabetes-induced elevation in the levels of IL-1beta, VEGF, and NF-B	[76]
Pycnogenol	Free radical scavenging; anti-inflammatory and capillary protective activities	[77]
Taurine	Multipotent activities prevent the changes in ultrastructure of retina and apoptosis in retinal glial cells; increasing activities of antioxidant enzymes and intracellular GSH	[78, 79]
Zinc	Reversed the depleting effect on retinal GSH	[80]