International Journal of Science and Research (IJSR)

International Journal of Science and Research (IJSR)
Call for Papers | Fully Refereed | Open Access | Double Blind Peer Reviewed

ISSN: 2319-7064

Downloads: 131 | Views: 250

Research Paper | Biochemistry Science | India | Volume 4 Issue 4, April 2015 | Rating: 6.8 / 10

Oxidative Stress and 3243 A/G Mitochondrial Dna Mutation In Maternally Inherited Type 2 Diabetes Mellitus

Utpal J. Dongre | Virendra G. Meshram | Shailesh Pitale

Abstract: The imbalance between the activities of antioxidant enzymes and free radicals gives rise to oxidative stress. Increased oxidative stress can induce other serious complications in diabetic patients. Mutations in mitochondrial DNA can cause oxidative stress and type 2 diabetes mellitus. Hence, the present study was undertaken to evaluate the levels of antioxidant enzymes, lipid peroxidation and mitochondrial DNA 3243 A/G mutation in families with a history of maternally inherited type 2 diabetes mellitus. Method This study included two diabetic families and one normal healthy family. The level of catalase, Mn/Fe SOD, Cu/Zn SOD, nitric oxide and malonaldehyde formation were studied via various biochemical standard methods. DNA isolation and mutation analysis were done as per standard protocols and methods. Result As compared to control samples, a significant decrease in the activities of catalase (family 1 p<0.01, family 2 p<0.01), Mn/Fe SOD (family 1 p<0.01, family 2 p< 0.05), Cu/Zn SOD (family 1 p<0.001, family 2 p<0.01) was observed. Significantly increased concentrations of malonaldehyde (family 1 p< 0.05, family 2 p<0.05) and nitric oxide (family 1 p<0.05, family 2 p<0.05) was also observed. Both diabetic families represent altered antioxidant enzymes status. This study corroborates an absence of the mutation. Conclusion High oxidative stress was shown in both the families with diabetes, but we did not find a mutation in mitochondrial DNA.

Keywords: Oxidative stress, Antioxidant Enzymes, Free Radicals, Mitochondrial DNA

Edition: Volume 4 Issue 4, April 2015,

Pages: 72 - 78

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