Impacts of Antioxidative System and Oxidative Stress on Progression of Diabetic Mellitus

Main Article Content

Thinnakorn Lao-ong
Kanokwan Jarukamjorn
Waranya Chatuphonprasert

Abstract

Abstract


Diabetes mellitus (DM) is a disorder associated with an increase of both oxidative stress and free radicals,and subsequently damage to cells and tissues. Normally, the body has defense systems for scavenging free radicalsand decreasing oxidative stress. The antioxidative systems consist of both enzymatic and non-enzymatic systems.The enzymatic system, particularly, plays an important role in free radical scavenging. Therefore, alterations ofgenes and enzymes related antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathioneperoxidase (GPx) are present in DM. Many studies have shown that expression of genes and activities of enzymesrelated antioxidants in diabetes patients and diabetes induced mice/rat are positively or negatively modified.However, at present, there is no strong evidence supporting how diabetes mellitus influences the antioxidativesystem and oxidative stress. These modifications depend on type of diabetes, developmental duration of diabetes,gender, age and the responses of cells and tissues against the disease stages. The different type and varieties ofdiabetes induced mice/rat strains also lead to different results. Therefore, understanding the regulatory mechanismof these genes and enzymes involved enzymatic system of antioxidation are necessary and important for futureinvestigation and treatment of diabetes.

Article Details

Section
Review Article

References

Akerblom HK, Knip M. Putative environmental factors in type 1 diabetes. Diabetes Metab Rev 1998; 14(1): 31-67.

Akerblom HK, Vaarala O, Hyöty H, et al. Environmental factors in the etiology of type 1 diabetes. Am J Med Genet 2002; 115(1): 18-29.

Bagi Z, Koller A, Kaley G. PPAR gamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with type 2 diabetes. Am J Physiol Heart Circ Physiol 2004; 286(2): 742-748.

Bhor VM, Raghuram N, Sivakami S. Oxidative damage and altered antioxidant enzyme activities in the small intestine of streptozotocin-induced diabetic rats. Int J Biochem Cell Biol 2004; 36(1): 89-97.

Dinçer Y, Akçay T, Ilkova H, et al. DNA damage and antioxidant defense in peripheral leukocytes of patients with type I diabetes mellitus. Mutat Res 2003; 527(1-2): 49-55.

Domínguez C, Ruiz E, Gussinye M, et al. Oxidative stress at onset and in early stages of type 1 diabetes in children and adolescents. Diabetes Care 1998; 21(10): 1736-1742.

Furukawa S, Fujita T, Shimabukuro M, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest 2004; 114(12): 1752-1761.

Gillespie KM. Type 1 diabetes: pathogenesis and prevention. CMAJ 2006; 175(2): 165-170.

Jarukamjorn K, Lao-ong T, Chatuphonprasert W. Diabetic induction in experimental mouse model. Thai Pharm Health Sci J 2011; 6(3): 229-239.

Kakkar R, Mantha SV, Radhi J, et al. Increased oxidative stress in rat liver and pancreas during progression of streptozotocin-induced diabetes. Clin Sci (Lond) 1998; 94(6): 623-632.

Kamper EF, Chatzigeorgiou A, Tsimpoukidi O, et al. Sex differences in oxidant/antioxidant balance under a chronic mild stress regime. Physiol Behav 2009; 98(1-2): 215-222.

Kilpatrick ES, Rigby AS, Atkin SL. Insulin resistance, the metabolic syndrome, and complication risk in type 1 diabetes: “double diabetes” in the diabetes control and complications trial. Diabetes Care 2007; 30(3): 707-712.

Koya D, Hayashi K, Kitada M, et al. Effects of antioxidants in diabetes-induced oxidative stress in the glomeruli of diabetic rats. J Am Soc Nephrol2003; 14(8 Suppl 3): 250-253.

Lesiuk SS, Czechowska G, Zimmer MS, et al. Catalase, superoxide dismutase, and glutathione per-oxidase activities in various rat tissues after carbon tetrachloride intoxication. J Hepato-biliary Pancreat Surg 2003; 10(4): 309-315.

Levy Y, Zaltzberg H, Amotz AB, et al. ß-Carotene affects antioxidant status in non-insulin-dependent diabetes mellitus. Pat physiol 1999; 6(3): 157-161.

Limaye PV, Raghuram N, Sivakami S. Oxidative stress and gene expression of antioxidant enzymes in the renal cortex of streptozotocin-induced diabetic rats. Mol Cell Biochem 2003; 243(1-2): 147-152.

Lowell BB, Shulman GI. Mitochondrial Dysfunction and type 2 Diabetes. Science 2005; 307: 384-387.

Maritim AC, Sanders RA, Watkins JB. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol 2003; 17(1): 24-38.

Matsunami T, Sato Y, Sato T, et al. Oxidative stress and gene expression of antioxidant enzymes in the streptozotocin-induced diabetic rats under hyperbaric oxygen exposure. Int J Clin Exp Pathol 2009; 3(2): 177-188.

Mayfield J. Diagnosis and classification of diabetes mellitus: new criteria. Am Fam Physician 1998; 58(6): 1355-1362.

Memisogullari R, Taysi S, Bakan E, et al. Antioxidant status and lipid peroxidation in type II diabetesmellitus. Cell Biochem Funct 2003; 21(3): 291-296.

Nandhini AT, Thirunavukkarasu V, Ravichandran MK, et al. Effect of taurine on biomarkers of oxidative stress in tissues of fructose-fed insulin-resist-ant rats. Singapore Med J2005; 46(2): 82-87.

Ozcan U, Cao Q, Yilmaz E, et al. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science2004; 306(5695): 457-461.

Peng H, Hagopian W. Environmental factors in the development of type 1 diabetes. Rev Endocr Metab Disord 2006; 7(3): 149-162.

Ramakrishna V, Jailkhani R. Oxidative stress in non-insulin-dependent diabetes mellitus (NIDDM) patients. Acta Diabetol 2008; 45(1): 41-46.

Rees DA, Alcolado JC. Animal models of diabetes mellitus. Diabet Med 2005; 22(4): 359-370.

Rizvi SI, Maurya PK. Alterations in antioxidant enzymes during aging in humans. Mol Biotechnol 2007; 37(1): 58-61.

Scibior D, Czeczot H. Catalase: structure, properties, functions. Postepy Hig Med Dosw (Online)2006; 60: 170-180.

Singh K, Kaur S, Kumari K, et al. Alterations in lipid peroxidation and certain antioxidant enzymes in different age groups under physiological conditions. J Hum Ecol 2009; 27(2): 143-147.

Song F, Jia W, Yao Y, et al. Oxidative stress, antioxidant status and DNA damage in patients withimpaired glucose regulation and newly diagnosed type 2 diabetes. Clin Sci (Lond) 2007; 112(12): 599-606.

Steppan CM, Bailey ST, Bhat S, et al. The hormone resistin links obesity to diabetes. Nature 2001; 409(6818): 307-312.

Strominger JL. Biology of the human histocompatibility leukocyte antigen (HLA) system and a hypoth-esis regarding the generation of autoimmune diseases. J Clin Invest1986; 77(5): 1411-1415.

Tantibhedhyangkul W. Regulatory T cells and type 1 diabetes. Siriaj Med J 2006; 58: 1074-1080.

Turk HM, Sevinc A, Camci C, et al. Plasma lipid peroxidation products and antioxidant enzyme activities in patients with type 2 diabetes mellitus. Acta Diabetol 2002; 39(3): 117-122.

Undlien DE, Lie BA, Thorsby E. HLA complex genes in type 1 diabetes and other autoimmune diseases. Which genes are involved. Trends Genet 2001; 17(2): 93-100.

Vainshtein BK, Melik-Adamyan WR, Barynin VV, et al. Three-dimensional structure of the enzyme catalase. Nature.1981; 293(5831): 411-412.

Venkateswaran S, Pari L. Antioxidant effect of Phaseolus vulgaris in streptozotocin-induced diabetic rats. Asia Pac J Clin Nutr 2002; 11(3): 206-209.

Weyer C, Tataranni PA, Bogardus C, et al. Insulin resistance and insulin secretary dysfunction are independent predictors of worsening of glucose tolerance during each stage of type 2 diabetes development. Diabetes Care 2001; 24(1): 89-94.

Wu H, Guo H, Zhao R. Effect of Lycium barbarumpolysaccharide on the improvement of antioxidant ability and DNA damage in NIDDM rats. Yakugaku Zasshi 2006; 126(5): 365-371.

Zelko IN, Mariani TJ, Folz RJ. Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and ex-pression. Free Radic Biol Med 2002; 33(3): 337-349.

Zotova EV, Savost’ianov KV, Chistiakov DA, et al. Association of polymorphic markers for genes coding for antioxidant defense enzymes, with development of diabetic polyneuropathies in patients with type 1 diabetes mellitus. Mol Biol (Mosk) 2004; 38(2): 244-249.