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      Gene polymorphisms of superoxide dismutases and catalase in diabetes mellitus


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          Reactive oxygen species generated by hyperglycaemia modify structure and function of lipids, proteins and other molecules taking part in chronic vascular changes in diabetes mellitus (DM). Low activity of scavenger enzymes has been observed in patients with DM. Protective role of scavenger enzymes may be deteriorated by oxidative stress. This study was undertaken to investigate the association between gene polymorphisms of selected antioxidant enzymes and vascular complications of DM.


          Significant differences in allele and genotype distribution among T1DM, T2DM and control persons were found in SOD1 and SOD2 genes but not in CAT gene (p < 0,01). Serum SOD activity was significantly decreased in T1DM and T2DM subjects compared to the control subjects (p < 0,05). SOD1 and SOD2 polymorphisms may affect SOD activity. Serum SOD activity was higher in CC than in TT genotype of SOD2 gene (p < 0,05) and higher in AA than in CC genotype of SOD1 gene (p < 0,05). Better diabetes control was found in patients with CC than with TT genotype of SOD2 gene. Significantly different allele and genotype frequencies of SOD2 gene polymorphism were found among diabetic patients with macroangiopathy and those without it. No difference was associated with microangiopathy in all studied genes.


          The results of our study demonstrate that oxidative stress in DM can be accelerated not only due to increased production of ROS caused by hyperglycaemia but also by reduced ability of antioxidant defense system caused at least partly by SNPs of some scavenger enzymes.

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          Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression.

          Superoxide dismutases are an ubiquitous family of enzymes that function to efficiently catalyze the dismutation of superoxide anions. Three unique and highly compartmentalized mammalian superoxide dismutases have been biochemically and molecularly characterized to date. SOD1, or CuZn-SOD (EC, was the first enzyme to be characterized and is a copper and zinc-containing homodimer that is found almost exclusively in intracellular cytoplasmic spaces. SOD2, or Mn-SOD (EC, exists as a tetramer and is initially synthesized containing a leader peptide, which targets this manganese-containing enzyme exclusively to the mitochondrial spaces. SOD3, or EC-SOD (EC, is the most recently characterized SOD, exists as a copper and zinc-containing tetramer, and is synthesized containing a signal peptide that directs this enzyme exclusively to extracellular spaces. What role(s) these SODs play in both normal and disease states is only slowly beginning to be understood. A molecular understanding of each of these genes has proven useful toward the deciphering of their biological roles. For example, a variety of single amino acid mutations in SOD1 have been linked to familial amyotrophic lateral sclerosis. Knocking out the SOD2 gene in mice results in a lethal cardiomyopathy. A single amino acid mutation in human SOD3 is associated with 10 to 30-fold increases in serum SOD3 levels. As more information is obtained, further insights will be gained.
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            Oxidative stress and the use of antioxidants in diabetes: Linking basic science to clinical practice

            Cardiovascular complications, characterized by endothelial dysfunction and accelerated atherosclerosis, are the leading cause of morbidity and mortality associated with diabetes. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Overproduction and/or insufficient removal of these free radicals result in vascular dysfunction, damage to cellular proteins, membrane lipids and nucleic acids. Despite overwhelming evidence on the damaging consequences of oxidative stress and its role in experimental diabetes, large scale clinical trials with classic antioxidants failed to demonstrate any benefit for diabetic patients. As our understanding of the mechanisms of free radical generation evolves, it is becoming clear that rather than merely scavenging reactive radicals, a more comprehensive approach aimed at preventing the generation of these reactive species as well as scavenging may prove more beneficial. Therefore, new strategies with classic as well as new antioxidants should be implemented in the treatment of diabetes.
              • Record: found
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              Mortality trends in men and women with diabetes, 1971 to 2000.

              Whether mortality rates among diabetic adults or excess mortality associated with diabetes in the United States has declined in recent decades is not known. To examine whether all-cause and cardiovascular disease mortality rates have declined among the U.S. population with and without self-reported diabetes. Comparison of 3 consecutive, nationally representative cohorts. Population-based health surveys (National Health and Nutrition Examination Surveys I, II, and III) with mortality follow-up assessment. Survey participants age 35 to 74 years with and without diabetes. Diabetes was determined by self-report for each survey (1971-1975, 1976-1980, and 1988-1994), and mortality rates were determined through 1986, 1992, and 2000 for the 3 surveys, respectively. Among diabetic men, the all-cause mortality rate decreased by 18.2 annual deaths per 1000 persons (from 42.6 to 24.4 annual deaths per 1000 persons; P = 0.03) between 1971 to 1986 and 1988 to 2000, accompanying decreases in the nondiabetic population. Trends for cardiovascular disease mortality paralleled those of all-cause mortality, with 26.4 annual deaths per 1000 persons in 1971 to 1986 and 12.8 annual deaths per 1000 persons in 1988 to 2000 (P = 0.06). Among women with diabetes, however, neither all-cause nor cardiovascular disease mortality declined between 1971 to 1986 and 1988 to 2000, and the all-cause mortality rate difference between diabetic and nondiabetic women more than doubled (from a difference of 8.3 to 18.2 annual deaths per 1000 persons). The difference in all-cause mortality rates by sex among people with diabetes in 1971 to 1986 were essentially eliminated in 1988 to 2000. Diabetes was assessed by self-report, and statistical power to examine the factors explaining mortality trends was limited. Progress in reducing mortality rates among persons with diabetes has been limited to men. Diabetes continues to greatly increase the risk for death, particularly among women.

                Author and article information

                BMC Med Genet
                BMC Medical Genetics
                BioMed Central
                21 April 2008
                : 9
                : 30
                [1 ]3rd Dept. of Internal Medicine, 1st Faculty of Medicine, Charles University, Prague, Czech Republic
                Copyright © 2008 Flekac et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 7 October 2007
                : 21 April 2008
                Research Article



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