Researchers from the University of Pittsburgh have uncovered new findings about the biology of telomeres, which were recently published in the journal Nature Structural and Molecular Biology.
According to the university, telomeres are composed of repeated sequences of DNA and they shorten every time a cell divides. This means that with age, they eventually stop dividing permanently, which contributes to aging-related diseases. In contrast, in most cancer cells, levels of the enzyme telomerase (which lengthens telomeres) are elevated. This is what enables them to divide indefinitely.
Previous studies have shown that oxidative stress accelerates telomere shortening. It also is known to play a role in inflammation and cancer, and damage from it is believed to build up during the aging process. The goal of this study was therefore to determine what happens to telomeres when they are damaged by oxidative stress.
The researchers suspected oxidative damage would render telomerase ineffective, but they found that telomerase could still lengthen telomeres with oxidative damage. In fact, the oxidative damage seemed to promote telomere lengthening, as the telomerase was able to add a damaged DNA precursor molecule to the end of the telomere. However, beyond the damaged precursor, it was unable to add additional DNA molecules.
These results suggest the mechanism by which oxidative stress accelerates telomere shortening is by damaging the DNA precursor molecules, not the telomere itself. This puts forth a new target for anti-inflammation and anti-aging therapies, not to mention cancer.