Determination of Mitochondrial Diversity Pattern in the Neutrophils of Normal Males

Abstract

Among the numerous theories that explain the process of aging, the mitochondrial theory of aging has received the most attention. This theory states that electrons leaking from the ETC (Electron Transfer Chain) reduce molecular oxygen to form superoxide anion radicals, through both enzymatic and non-enzymatic reactions, can cause the generation of other ROS (reactive oxygen species). The ensuing state of oxidative stress results in damage to ETC components and mtDNA (mitochondrial DNA), thus increasing further the production of ROS. Ultimately, this „vicious cycle‟ leads to a physiological decline in function, or aging. Neutrophils, the primary phagocytic cells of the human immune system, have a very short life span after leaving the bone marrow of approximately 24 hours. Thereafter, they die either by intrinsically or extrinsically induced apoptosis. Intrinsically, neutrophil apoptosis appears to be regulated at the level of their mitochondria. In the present study, age group ranging from 21 to 55 were taken for the blood profiling, serum biochemical parameters and mitochondrial proteins and enzyme activity determination studies of normal healthy men. In the present study, neutrophil has been used as the somatic cell representative. The results show that the values of blood profiling parameters and serum biochemical levels did not show any trend and was found to be fluctuating within the normal range. Antioxidants assay were performed which revealed a decline in the mitochondrial SOD and Catalase activities with increasing age. The activities of the other mitochondrial enzymes, Succinate dehydrogenase and Malate dehydrogenase have shown variations in the neutrophil. RINKAL MEHTA 2010-2011 Page 10 It can be thus concluded that there is a gradual decline in most of the mitochondrial antioxidant levels and enzymes with increase in age. The same needs to be confirmed with the mitochondrial apoptotic marker enzymes. The polymorphism found in the mitochondrial enzymes of neutrophil can be further checked at the genetic levels. And the variations obtained can be co-related with mitochondrial dysfunctioning and mitochondrial associated neurodegenerative diseases with age as parameter.