Figure 4: Hypothetic model of oxidative stress and carbonyl lesions in ulcerative colitis and associated colorectal cancer. Infection and immune response act as primary initiators to trigger inflammation and inflammatory cell infiltration. In this process, intestinal mucosal crypt abscesses occur and vast reactive oxygen species (ROS) are produced, thus leading to oxidative stress. Excessive ROS exaggerate inflammatory lesions and stimulate epithelial cell proliferation through oxidative insults to proteins, lipids, and DNA and also by activation of cell signaling pathways, eventually leading to ulcerative colitis (UC) and colitis-associated colorectal cancer (CAC). Electrophilic carbonyl compounds play as important secondary factors of oxidative stress to cause cellular and macromolecular lesions, which, together with oxidative stress, may form a vicious cycle. Meanwhile, proinflammatory cytokines produced by epithelial cells and infiltrated inflammatory cells may promote the progression of UC and CAC.