A team of researchers from the University of Pittsburgh, lead by Patricia Opresko, Ph.D have discovered crucial new information about telomeres, the end caps of DNA. Telomeres (repeated sequences of DNA) are shortened each time a cell divides, thus becoming smaller with age. When telomeres become too short, they send a signal to the cell to cease dividing permanently – this impairs the ability of tissues to regenerate, contributing to various age-related diseases.
In cancer cells, on the other hand, levels of the enzyme telomerase (which lengthens telomeres) are elevated. This enables them to divide indefinitely. “The new information will be useful in designing new therapies to preserve telomeres in healthy cells and ultimately help combat the effects of inflammation and aging. On the flip side, we hope to develop mechanisms to selectively deplete telomeres in cancer cells to stop them from dividing,” said Dr. Opresko.
Previous studies have shown that oxidative stress accelerates telomere shortening. Oxidative stress is a condition where free radicals build up inside the cell, causing damage. Free radicals can damage the DNA that makes up the telomeres, as well as the DNA building blocks used to extend them. Oxidative stress also plays a role in various other health conditions, including cancer and inflammation. Free radical damage, which is often caused by inflammation in the body, as well as environmental factors, is believed to build up throughout the aging process.