SERUM NOx AND RBC LYSATE SOD LEVELS IN DIABETIC PATIENTS AND THEIR RELATION WITH DURATION OF DIABETES MELLITUS

Authors

  • Renuka P
  • NAVEEN CR

Abstract

 

 Objective: Oxidative stress is one of the major causes for complications in diabetic patients. Oxidative stress might be due to an imbalance in elimination and production of free radicals. Nitric oxide (NO) is a reactive oxygen species (RNS) and a potent vasodilator. When NO reacts with superoxide anion, it forms RNS. Superoxide dismutase (SOD) is an antioxidant enzyme which eliminates O2–.

Methods: In the present study, 53 diabetic patients have been selected randomly and grouped into two groups based on the diabetic duration to evaluate the effect of duration on oxidative stress.

Results: Red blood cells lysate SOD (4.745±1.047) and serum NO (52.2±25.8) are increased in diabetic patients compared with healthy controls. However, when compared between groups of different diabetic duration, SOD is decreased whereas NO is increased.

Conclusion: Decrease in SOD activity might be due to the loss of its activity by glycation, whereas increase in NO might be due to the induction of endothelial NO synthase by glucose.

Keywords: Diabetes mellitus, Nitric oxide, Oxidative stress, Superoxide dismutase.

INTRODUCTION

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References

Ceriello A. Oxidative stress and glycemic regulation. Metabolism 2000;49 2 Suppl 1:27-9.

Baynes JW, Thorpe SR. Role of oxidative stress in diabetic complications: A new perspective on an old paradigm. Diabetes 1999;48(1):1-9.

Baynes JW. Role of oxidative stress in development of complications in diabetes. Diabetes 1991;40(4):405-12.

Halliwell B, Gutteridge JM. Free radicals and toxicology. In: Free Radicals in Biology and Medicine. Oxford: Clarendon Press; 1997. p. 1-27.

Mehran MJ, Zendehbad H, Malla S. Free radical scavenging and antioxidant potential activity of cassava plants. Asian J Pharm Clin Res 2014;7 Suppl 1:66-70.

Arya A, Aggarwal S, Yadav HN. Pathogenesis of diabetic nephropathy. Int J Pharm Pharm Sci 2010;2 Suppl 2:24-9.

Kar S, Kavdia M. Local oxidative and nitrosative stress increases in the microcirculation during leukocytes-endothelial cell interactions. PLoS One 2012;7(6):e38912.

Naveen CR, Renuka P. Nitric oxide in diabetic patients and its relation with HbA1c. Int J Pharm Clin Res 2014;6(2):146-8.

Satoh M, Fujimoto S, Haruna Y, Arakawa S, Horike H, Komai N, et al. NAD(P) H oxidase and uncoupled nitric oxide synthase are major sources of glomerular superoxide in rats with experimental diabetic nephropathy. Am J Physiol Renal Physiol 2005;288(6):F1144-52.

Kimura F, Hasegawa G, Obayashi H, Adachi T, Hara H, Ohta M, et al. Serum extracellular superoxide dismutase in patients with type 2 diabetes: Relationship to the development of micro-and macrovascular complications. Diabetes Care 2003;26(4):1246-50.

Kawamura N, Ookawara T, Suzuki K, Konishi K, Mino M, Taniguchi N. Increased glycated Cu, Zn-superoxide dismutase levels in erythrocytes of patients with insulin-dependent diabetis mellitus. J Clin Endocrinol Metab 1992;74(6):1352-4.

Huie RE, Padmaja S. The reaction of no with superoxide. Free Radic Res Commun 1993;18(4):195-9.

Li W, Yanoff M, Jian B, He Z. Altered mRNA levels of antioxidant enzymes in pre-apoptotic pericytes from human diabetic retinas. Cell Mol Biol (Noisy-le-grand)1999;45(1):59-66.

Lee HY, Noh HJ, Gang JG, Xu ZG, Jeong HJ, Kang SW, et al. Inducible nitric oxide synthase (iNOS) expression is increased in lipopolysaccharide (LPS)-stimulated diabetic rat glomeruli: Effect of ACE inhibitor and angiotensin II receptor blocker. Yonsei Med J 2002;43(2):183-92.

Published

01-11-2014

How to Cite

P, R., and N. CR. “SERUM NOx AND RBC LYSATE SOD LEVELS IN DIABETIC PATIENTS AND THEIR RELATION WITH DURATION OF DIABETES MELLITUS”. Asian Journal of Pharmaceutical and Clinical Research, vol. 7, no. 5, Nov. 2014, pp. 220-1, https://mail.innovareacademics.in/journals/index.php/ajpcr/article/view/2642.

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