Several human cancers are associated with chronic bacterial, viral and parasitic infections. Nitric oxide, which is a short-lived free radical produced by many types of cells for a number of important physiological functions, is elevated in these infections. Long-term exposure to elevated NO. in cells could have potential genotoxic effects on hosts. There are at least three mechanisms by which intracellular elevated NO. could exert genotoxic affects after reacting with O2. These include formation of carcinogenic N-nitroso compounds, direct deamination of DNA bases, and oxidation of DNA after formation of peroxynitrite and/or hydroxyl radicals. One or more of these mechanisms could, theoretically, explain why chronic infection increases the risk of certain cancers.