Cells are continuously threatened by the damage caused by reactive oxygen/nitrogen species (ROS/RNS), which are produced during physiological oxygen metabolism. In our review, we will summarize the latest reports on the role of oxidative stress and oxidative stress-induced signaling pathways in the etiology of colorectal cancer. The differences in ROS generation may influence the levels of oxidized proteins, lipids, and DNA damage, thus contributing to the higher susceptibility of colon. Reactive species (RS) of various types are formed and are powerful oxidizing agents, capable of damaging DNA and other biomolecules. Increased formation of RS can promote the development of malignancy, and the "normal" rates of RS generation may account for the increased risk of cancer development in the aged. In this review, we focus on the role of oxidative stress in the etiology of colorec-tal cancer and discuss free radicals and free radical-stimulated pathways in colorectal carcinogenesis.