Research Projects

Oxidative damage markers of DNA, Lipid and Protein (OS) do not increase with increase in the risk factors of MetS but is definitely high in those diagnosed with MetS compared to those without the syndrome. There is a cumulative and synergistic effect of the risk factors of MetS, 3 or more risks of MetS induces a greater degree of OS. However, presence of even a single risk factor of MetS can increase OS. There was an increased DNA damage in MetS despite maximum Antioxidant Capacity. The Reactive Oxygen Species “H2O2” may increase with increase in the fat depots of the body but then the use of H2O2 alone as an OS stress marker may not be enough. The indirect but more stable markers, comprising of Advanced Glycation End Product, Advanced Oxidation Protein Product, Protein Carbonyl, Malondialdehyde,, 4- Hydroxynonenal, DNA/RNA oxidative damage and even DNA strand break can be used as a surrogate marker for Oxidative stress in MetS but oxidative DNA damage marker would be more appropriate. In an OS scenario, DNA damage is always more than Lipids and Proteins. The DNA molecule is not only damaged by the ROS like H2O2,but the resultant products generated on oxidative damages to Proteins and Lipids incorporates additional damage to increase the damage load. If DNA damage continues and supersedes the cells last resort of repair which is the DNA repair mechanism likelihood of unfavorable complications due to cell death and future acquired carcinogenesis can increase tremendously.