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Oxidative stress to DNA increases with age, study finds

The older a rodent is, the greater the chance that its genes have been damaged by oxidation. That's the conclusion of a study conducted at The University of Texas Health Science Center at San Antonio (UTHSC) and published in the Aug. 21 issue of the Proceedings of the National Academy of Sciences-USA.

The researchers compared levels of a key stress marker, 8-oxo-2-deoxyguanosine (oxo8dG), in rats and mice of various ages. The scientists scanned liver, kidney, brain, heart and muscle tissue, finding that the older the rat or mouse, the higher the level of the marker. Oxo8dG is described as a modification of a genetic sequence.

One theory of aging is that oxidants are generated during normal metabolism and can react with DNA, the genetic code, causing damage. The body continuously repairs its own DNA, but any oxidative lesion that is not repaired can lead to mutations, increasing the risk of cancer.

This study suggests that the age-related increase in oxidative lesions in DNA could be an important factor in the age-related increase in most cancers. Age is well documented to be the leading risk factor for most cancers.

The study was part of a Ph.D. dissertation written by Michelle Hamilton, a graduate student in the UTHSC department of physiology, with assistance from her mentor, Arlan G. Richardson, Ph.D., and other faculty members in the Sam and Ann Barshop Center on Longevity and Aging Studies, the departments of physiology and cellular and structural biology, and the Geriatric Research, Education and Care Center at the South Texas Veterans Health Care System, Audie Murphy Division.

Contact: Will Sansom