Two Theories Linking DNA Damage and Aging: Free Radical/Oxidation vs. Telomere Shortening
Ruwaida Dhala-Vakil, BSc, MSc
There are many factors involved in human aging, and significant progress has been made in this field over the last few decades. Recent evidence from cloned calves suggests that scientists may not merely be able to reverse the cellular damage accumulating with age--they may, in fact, be able to prolong cell life. The cells from these cloned animals lived longer in culture and had longer telomeres than their normal counterparts. If this extension of the cellular life span can be translated into longer life for the entire organism, the calves may live fifty percent longer than normal.1 Additionally, studies on antioxidants show that transgenic Drosophila (the fruit fly), which overexpress antioxidant genes, live 34% longer than controls.2 This article will focus on both the free radical/oxidation theory of aging, and the role of telome-rase in aging.
Free Radical/Oxidation Theory of Aging
In 1956, Denham Harman suggested that there is an age-related accumulation of reactive oxygen species (ROS) which causes damage to cellular components. The damage is targeted to the proteins and DNA in the nucleus and mitochondria, as well as to the proteins and lipids in the cell membrane, and the proteins of the cytoplasm. Mitochondrial DNA is located near the inner mitochondrial membrane, close to the sites where free radicals form.
