Lipid Peroxidation–Derived DNA Adducts and the Role in Inflammation‐Related Carcinogenesis

Chronic infection and persistent inflammation are now recognized as important risk factors in many human cancers. Emerging evidence suggests that cancer-related inflammatory processes cause tissue damage and genetic instability involved in the initiation, promotion, and progression of carcinogenesis. Reactive oxygen (ROS) and nitrogen (RNS) species and lipid peroxidation (LPO)–mediated tissue damage play a major role in inflammation-related malignancies. This chapter provides information on methods for quantifying some representative lipid peroxidation (LPO)-derived DNA adducts in human biomonitoring studies. It summarizes results from biomarker applications that have provided insights intomechanisms of cancer causation and possibilities of preventive measures in human at risk subjects. Data compiled in this chapter provide evidence that persistent oxidative/nitrative stress and excess LPO are induced by chronic inflammatory processes and infections, causing massive DNA damage from endogenous sources.