Impaired Antioxidant Defence Mechanism In Diabetic Retinopathy
3429-3436
Correspondence
Dr T Vivian Samuel MD
Reader, Department of Biochemistry,
JJM Medical College,
Davangere – 577004,
Karnataka.
Mob no: 9448028229
e-mail: tviviansamuel@yahoo.co.in
Background
Oxidative stress resulting from enhanced free-radical formation and a defect in antioxidant defences, has been implicated in the pathogenesis of diabetes and its complications include neuropathy, retinopathy, nephropathy, etc.
Aims
The aim of the present study was to evaluate the levels of selected oxidation and the antioxidant status with relevance to diabetic retinopathy and to correlate the antioxidant status with glycaemic control.
Materials and Methods
Thirty patients of type-2 diabetes mellitus (DM) without retinopathy, 30 patients of diabetic retinopathy and 30 normal subjects were included in this study. The degree of lipid peroxidation in terms of serum malondialdehyde (MDA) by the thiobarbituric acid method along with antioxidant defences, erythrocyte superoxide dismutase (SOD), reduced glutathione (GSH) and serum vitamin C was estimated in healthy controls and non-insulin dependent diabetes mellitus (NIDDM) subjects with and without retinopathy. Fasting blood glucose was also estimated and correlated with the antioxidant status. The statistical analysis was done by using the Students unpaired ‘t’ test and the correlation was done by using Pearson's correlation coefficient.
Results
The levels of serum MDA were found to be increased significantly in the diabetic retinopathy cases as compared to those in the cases with diabetes without retinopathy and in the healthy controls. The levels of superoxide dismutase (SOD), reduced glutathione (GSH) and vitamin C were significantly reduced in all diabetic patients, i.e., those with and without retinopathy. However, the lowest levels were found in the diabetic patients with retinopathy. A negative correlation was found between FBS and antioxidant enzymes in the diabetic retinopathy cases.
Conclusion
The results suggest that antioxidant deficiency and excessive peroxidation damage appear in NIDDM, and the severity is more with the development of complications. Therapeutic measures to increase the antioxidants and to control lipid peroxidation are warranted for the effective control of its complications.