Iron supplementation may aggravate inflammatory status of colitis in a ratmodel

Iron supplementation is one of the principal therapies in in inflammatory b owel disease. Iron is a major prooxidative agent; therefore therapeutic iro n as well as heme iron from chronic mucosal bleeding can increase the iron- mediated oxidative stress in colitis by facilitating the Fenton reaction, n amely production of hydroxyl radicals. In the present study colitis was ind uced in the iodoacetamide rat model. Forty male Whistar rats were divided i nto four groups, each group receiving a different diet regimen in parallel with colitis induction: Malondialdehyde was measured to assess the degree o f tissue oxidative stress. There were microscopic changes, and significantl y more severe colitis was seen in colonic biopsies when iron was supplement ed. It was concluded that iron supplementation can amplify the inflammatory response and enhance the subsequent mucosal damage in a rat model of colit is. We suggest that the resultant oxidative stress generated by iron supple mentation leads to the extension and propagation of crypt abscesses.