The molecular epidemiology of oxidative damage to DNA and cancer

Abstract

Oxygen is required for respiration and the energetic processes that enable aerobic life. A cost associated with oxygen use is free-radical formation, which damages genome stability and contributes to various processes including aging, degenerative diseases, and cancer (1,2). Foods including fruits, vegetables, tea components, and trans-fats; nutrients including vitamins C and E, selenium, beta-carotene, and dietary fish oil; chemotherapeu-tic drugs; radiation; infection; environmental exposures includ-ing air pollution; and hereditary and acquired conditions broadly contribute to or oppose free-radical formation and genomic dam-age (2–9). Individually and cooperatively, the action of modu-lators of oxidative DNA damage is the focus of intense study and controversy (10). Understanding the regulation of free-radical formation and its consequences may provide new insight into the etiology of cancer and lead to the development of effectiv