New observations of (1) colitis-by-association, (2) the carriage of nitric oxide by haemoglobin, (3) nitric oxide inactivation of CoA, (4) the damage caused to colonocytes by a combination of nitric oxide/sulphide/hydrogen peroxide and (5) colonic extraction of nitric oxide from the circulation, has led to new views on colonocyte damage in colitis. These observations should assist to define initiating factors that lead to release of damaging agents (nitric oxide/hydrogen peroxide) and to delineate protective mechanisms against colonocyte damage. Overall, the production, release, disposal and inactivation of nitric oxide are related to damage to colonocytes and consequent ulceration in colitis.
Copyright 2002 S. Karger AG, Basel