A team of researchers led by Patricia Opresko, PhD, Associate Professor of Environmental and Occupational Health at Pitt, and member of the UPCI Molecular and Cellular Cancer Biology Program and Carnegie Mellon University Center for Nucleic Acids Science and Technology, has uncovered new details about the biology of telomeres. These DNA “caps” protect the tips of chromosomes and play key roles in a number of health conditions, including cancer, inflammation and aging. Telomeres are shortened every time a cell divides and therefore become smaller as a person ages. When they become too short, telomeres send a signal to the cell to stop dividing permanently, which impairs the ability of tissues to regenerate and contributes to many aging-related diseases. In contrast, in most cancer cells, levels of the enzyme telomerase, which lengthens telomeres, are elevated, allowing them to divide indefinitely.
A number of studies have shown that oxidative stress—a condition where damaging molecules known as free radicals build up inside cell—accelerates telomere shortening. Free radicals can damage not only the DNA that make up telomeres, but also the DNA building blocks used to extend them. New findings by the research team suggest that the mechanism by which oxidative stress accelerates telomere shortening is by damaging the DNA precursor molecules, not the telomere itself. Mediation of these biological activities may provide new approaches for treating cancer.