Correlation of Protein Carbonyl and Malondialdehyde in Oxidative Stress Induced Senescence of RBC Membrane in Type 2 Diabetes Mellitus
Diabetes mellitus is a group of metabolic disease characterised by a state of chronic hyperglycemia. The biochemical process of Advanced Glycation appears to be enhanced in the Diabetes melieu as a result of not only hyperglycemia but also other stimuli such as oxidative stress and lipid peroxidation. The aim of the study is to establish a link between the oxidative stress induced by changes with protein carbonyl content and MDA damaging the RBC membrane composition in Type 2 DM in comparison to normal controls. The correlation of Malondialdehyde (MDA) and Protein carbonyl levels in relation to control of Type 2 Diabetes mellitus based on HbA1C level indicate that there is an autooxidation of glucose which results in persistent production of malondialdehyde(MDA) and ROS which can release advance glycation end products (AGE) and advanced lipoxidation end products(ALE) along with increased carbonylation of proteins leading to protein damage, oxidative modification of aminoacid residues ,aminoacid fragmentation and increased proteolytic susceptibility. Protein carbonyl can be generated by via non specific oxidation of aminoacid by via nonspecific oxidation of aminoacid or via catalysed oxidation of specific aminoacid key to protein function by oxygen and glycation. A case control comparative study was done with Type 2 Diabetes mellitus and normal controls at BMCH & RC, chitradurga. According to the criteria, blood sample were collected under aseptic precautions and evaluation of fasting blood sugar, HbA1C, Protein carbonyl along with RBC membrane ghost preparation and estimation of malondialdehyde(MDA) were done. It was found that there was significant increase of protein carbonyl in serum of Type2 DM cases (1.20±0.08) in comparison to control groups (0.90±0.06) with a statistical significance of (p<0.001) along with Malondialdehyde (MDA) of RBC membrane which was also significantly increased (4.23±0.21) in Type 2 Diabetes Mellitus in comparison to normal control (3
