FRIDAY, Sept. 5, 2003 (HealthDayNews) -- A defect in the body's self-defense mechanism against age-related genetic mutations has been identified by researchers at the University of Texas Medical Branch at Galveston.
The finding may help explain why the aging human body can't defend itself against DNA damage in the mitochondria, the power plants that fuel the growth and activity of cells.
Finding ways to help aging cells repair their own damaged DNA could possibly lead to ways to prevent or treat cancer, Alzheimer's disease, Parkinson's disease and other health problems caused by genetic defects.
As cells age, they experience continuous genetic mutations, some of which are caused by the harmful byproducts of the oxygen we inhale. But the body's repair mechanism is constantly at work fixing this DNA damage. However, this repair activity becomes less efficient as cells age.
In this study, the researchers analyzed why this DNA repair activity becomes less effective in the mitochondria as cells age. They found a biochemical "roadblock" that prevents much of the repair enzyme activity from reaching the site of the DNA damage in the mitochondria of aging cells.
In old cells, about half of the repair enzyme activity can't reach the mitochondria DNA to repair it.
The study was published online this week in the Proceedings of the National Academy of Sciences.
Here's where you can learn more about cells.