Experimental colitis is associated with ultrastructural changes in inflamed and uninflamed regions of the gastrointestinal tract.

Objectives: The objective of this study was to examine the ultrastructural changes in cell organelles such as mitochondria, endoplasmic reticulum (ER) and Golgi apparatus in inflamed colon and uninflamed ileum in colitic rats.

Materials And Methods: Colitis was induced in rats by intracolonic administration of trinitrobenzenesulfonic acid (TNBS). The animals were sacrificed on day 5 after TNBS administration and colonic and ileal samples were used for estimation of myeloperoxidase (MPO) activity, malondialdehyde (MDA) concentration, histologic examination and transmission electron microscopy.

Results: TNBS caused a significant reduction in body weight and an increase in MPO activity in colonic, but not in the ileal samples in animals with colitis. MDA levels were increased both in inflamed colon and the uninflamed ileal segments in colitis. Electron microscopy revealed swelling of mitochondria with broken cristae and disruption of the inner membrane. Colitis also caused fragmentation of the ER with loss of ribosomes and swelling of the Golgi apparatus with distended vesicles in both smooth muscle and epithelial cells in the ileal and colonic segments. These changes were absent in the control rats without colitis.

Conclusions: These findings demonstrate ultrastructural deformities in both the mucosa and smooth muscle in inflamed and uninflamed regions of the gastrointestinal tract in experimental colitis. The structural changes in mitochondria are responsible for reduced ATP, while abnormalities in the ER and the Golgi apparatus may explain a generalized effect on protein synthesis, trafficking and targeting mechanisms, and may account for physiological changes seen in experimental colitis.