Antioxidant Status of Nigerians with Diabetic Disorders
[1]
Genesis YR, Department of Chemical Pathology, University of Maiduguri, Nigeria.
[2]
Ezimah ACU, Department of Physiology, Federal University Ndufu-Alike Abakaliki, Nigeria.
[3]
Ugwushi C, Department of Physiology, Federal University Ndufu-Alike Abakaliki, Nigeria.
[4]
Odo P, Department of Physiology, Federal University Ndufu-Alike Abakaliki, Nigeria.
[5]
Ajugwo AO, Department of Haematology and Blood Transfusion, Madonna University Elele, Nigeria.
During the past few years, identification of many molecules that participate in cellular processes has contributed to the information on pathogenesis in many non-communicable diseases. The present study was undertaken to evaluate total antioxidant status (TAS) as a factor in the pathogenesis of diabetes mellitus. The study included 88 diabetic patients and 30 apparently healthy non-diabetic controls. On the basis of biochemical attributes, the different types of diabetics in the study groups were gestational diabetes mellitus GDM (22%), insulin dependent diabetes mellitus IDDM (23%), and non-insulin dependent diabetes mellitus NIDDM (55%). Blood glucose levels and plasma total antioxidant status were determined using standard methods. Plasma total antioxidant status levels were significantly lower in the diabetic groups than in controls (p<0.05). This finding was independent of the type of diabetes. On comparative basis, the lowest value of TAS was predominantly found amongst the IDDM. In this study, plasma TAS levels are markedly reduced in patients with all types of diabetes and hence an indication of the involvement of reactive oxygen species in the pathogenesis of diabetes and can be used as a prognostic marker in diabetic patients.
Diabetic Disorders, Antioxidant Status, Pathogenesis, Oxidative Stress
[1]
Kalra, J., Mantha, S. V. and Prasad, K. (1994). Oxygen-free radicals: Key factors in Clinical Diseases. Labmedica International. 11(2): 16 – 21.
[2]
Lemens, C. and Sterrit, C. (2003). Treatment Issues. Gay Men’s Health Crisis. New York.
[3]
Diplock, A. (1991). Antioxidant nutrients and disease prevention: an overview. American Journal of Clinical Nutrition. 53: 189S – 193S.
[4]
Fidelus, R. K. (1986). Enhancement of intracellular glutathione promotes lymphocyte activation by motogen. Cellular Immunol. 97: 155 – 163.
[5]
Freeman, B. A. and Crapo, J. D. (1982). Biology of disease – free radicals and tissue injury. Lab. Invest. 47: 412 – 426.
[6]
Meerson, F. Z., Kagen, V. E. and Kezlor, Y. P. (1982). The role of lipid peroxidation in pathogenesis of ischemic damage and antioxidant protection of the heart. Basic Res. Cardiol. 77: 465 – 485.
[7]
Brooker, C. (2003). Pocket Medical Dictionary. Churchill Livingstone. Edinburgh. 89.
[8]
Miller, N. J., Rice-Evans, C., Davies, M. J., Gopinathan, V. and Milner, A. (1993). Clinical Sciences. 84: 407 – 412.
[9]
Chatfield, C. (1983). Statistics for Technology. 3rd Edition. Chapman and Hall London.
[10]
Zhao, L. (2001). Effects of free radicals in diabetes. Monograph. 4 – 12.
[11]
Bayness, J. W. (1991). Role of oxidative stress in the development of complications of diabetes. Diabetes. 40: 405 – 412.
[12]
Collins, A. R. (2005). Assays for oxidative stress and antioxidant status: applications to research into the biological effectiveness of polyphenols. Am. J. Clin. Nutr. 81(1 Suppl):261S - 267S.
[13]
Loft, S., Møller, P., Cooke, M. S., Rozalski, R. and Olinski, R. (2008). Antioxidant vitamins and cancer risk: is oxidative damage to DNA a relevant biomarker? Eur. J. Nutr. 47 (2):19 – 28.
[14]
Herbert, K. E., Fletcher, S., Chauhan, D., Ladapo, A., Nirwan, J., Munson, S. and Mistry, P. (2006). Dietary supplementation with different vitamin C doses: no effect on oxidative DNA damage in healthy people. Eur. J. Nutr. 45(2):97 – 104.
[15]
Moller, P., Viscovich, M., Lykkesfeldt, J., Loft, S., Jensen, A. and Poulsen, H. E. (2004). Vitamin C supplementation decreases oxidative DNA damage in mononuclear blood cells of smokers. Eur. J. Nutr. 43(5):267 – 274.
[16]
Blasiak, J., Arabski, M., Krupa, R., Wozniak, K., Zadrozny, M., Kasznicki, J., Zurawska, M. and Drzewoski, J. (2004). DNA damage and repair in type 2 diabetes mellitus. Mutat. Res. 554(1-2):297 – 304.
