Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 28, 2005; 11(16): 2371-2384
Published online Apr 28, 2005. doi: 10.3748/wjg.v11.i16.2371
Radical induction theory of ulcerative colitis
Jay Pravda
Jay Pravda, PO Box 142181, Gainesville, FL 32614, USA
Author contributions: All authors contributed equally to the work.
Correspondence to: Jay Pravda, MD, PO Box 142181, Gainesville, FL 32614, USA.
Telephone: +1-352-598-8866
Received: June 30, 2004
Revised: July 2, 2004
Accepted: July 15, 2004
Published online: April 28, 2005

To propose a new pathogenesis called Radical Induction to explain the genesis and progression of ulcerative colitis (UC). UC is an inflammatory bowel disease. Colonic inflammation in UC is mediated by a buildup of white blood cells (WBCs) within the colonic mucosal lining; however, to date there is no answer for why WBCs initially enter the colonic mucosa to begin with. A new pathogenesis termed “Radical Induction Theory” is proposed to explain this and states that excess un-neutralized hydrogen peroxide, produced within colonic epithelial cells as a result of aberrant cellular metabolism, diffuses through cell membranes to the extracellular space where it is converted to the highly damaging hydroxyl radical resulting in oxidative damage to structures comprising the colonic epithelial barrier. Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens from invading the normally sterile submucosa. This antigenic exposure provokes an initial immune response of WBC infiltration into the colonic mucosa. Once present in the mucosa, WBCs are stimulated to secrete toxins by direct exposure to fecal bacteria leading to mucosal ulceration and bloody diarrhea characteristic of this disease.

Keywords: Ulcerative colitis, Radical induction, Oxidative stress, Hydrogen peroxide