Abstract
Oxidative stress has been frequently associated with the development of type 2 diabetes mellitus. Manganese superoxide dismutase (MnSOD) is one of the most important enzymes responsible for the defense against oxidative damage in the mitochondria. A polymorphism in the second exon of the MnSOD at position 16 that changes Ala into Val, induces changes in the structural conformation and mitochondrial transport of MnSOD. This polymorphism affects the scavenger activity of the enzyme and generates high reactive oxygen species which could exacerbate the development of type 2 diabetes and/or its complications. Relationship between MnSOD polymorphism and Type 2 diabetes mellitus and its complications remains uncertain.
Highlights
Free radical-induced damage plays a significant role in the development of insulin resistance which is the main contributor to type 2 diabetes mellitus [1,2]
To investigate the susceptibility of patients with MnSODAla16Val with type 2 diabetes, 59 patients and 40 control subjects were recruited to the study; their genomic DNA was extracted followed by a direct polymerase chain reaction (PCR)-genotype analysis
Results show that the frequency of Manganese superoxide dismutase (MnSOD) single nucleotide polymorphism (SNP) showed that MnSOD Ala16Val genotype polymorphism was significantly associated with type 2 diabetes mellitus (T2DM) (Table 2)
Summary
Free radical-induced damage plays a significant role in the development of insulin resistance which is the main contributor to type 2 diabetes mellitus [1,2]. Antioxidant enzymes play an important role in limiting this oxidative stress burden and low activity of scavenger enzymes has been observed in patients with type 2 diabetes mellitus [3]. Antioxidant enzymes protect against the rapid onset and progression of diabetic complications such as diabetic neuropathy, diabetic nephropathy and cardio-vascular complications, by reducing the excess of highly reactive free radicals. The excess generation of reactive free radicals due to chronic hyperglycemia causes oxidative stress which further exacerbates the development and progression of diabetes and its complications through modification of various cellular events in many tissues, including vessels, kidney, pancreatic beta cells and liver [7]
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