Gastrointestinal mucosa is continuously exposed to endogenous and exogenous reactive oxygen species and oxidative damage has been associated with the etiology of digestive diseases [1]. In particular, iron ion-induced lipid peroxidation has been suggested as playing an important role in the development of colon cancer [2][3][4][5]. It was demonstrated that feces are a rich source of superoxide anion and hydrogen peroxide, which in conjunction with iron ions, generates hydroxyl radicals (HO ž ) through the Fenton reaction ( fig. 1) [2]. Feces are known to contain high amounts of iron ions, since dietary iron is poorly absorbed in the small intestine. HO ž formed in this way within the colon attacks compounds present in or near the site of its formation. Apart from its role in mediating several carcinogenic mechanisms such as hydroxylation reactions, HO ž initiates lipid peroxidation with the formation of phospholipid hydroperoxides in cell membranes. In the presence of metal ions, phospholipid hydroperoxides generate lipid alkoxyl or peroxyl radicals that further propagate the lipid peroxidation chain reaction [6]. This propagative lipid peroxidation extensively damages cell membranes and other important biomolecules, resulting in tissue injury ( fig. 1).Like other tissues, gastrointestinal mucosa is protected by enzymatic and nonenzymatic antioxidant systems. Several studies demonstrated the differences in the distribution of antioxidant compounds and antioxidant enzymes along the gastrointestinal tract, which are probably correlated with the susceptibility of the gastrointestinal tract to oxidative stress [7,8]. In order to understand the differences in tissue susceptibility to oxidative stress in gastrointestinal tract, this study aimed to characterize the oxidizability of large intestinal mucosa in iron ion-induced lipid peroxidation and to compare its mucosal peroxidizability with those of the stomach and small intestine.