Changes in Plasma and Colonic Mucosa Fatty Acid Pro®les in Rats with Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid N. NIETO, PhD, M.D. GIRON, PhD, M.D. SUAREZ, PhD, and A. GIL, PhD Polyunsaturate d fatty acids have a key role in the pathoge nesis of in¯ammatory bowel disease since some of the arachidonic acid-de rived eicosanoids have been found to be increased in in¯amed intestinal mucosa in the acute phase of human disease. The aim of this study was to prospectively assess plasma and colon mucosa fatty acid patterns in rats with experimental ulcerative colitis. Twenty rats were treated with trinitrobenzene sulfonic acid and 20 with NaCl; two groups were killed after one week and two after two weeks to evaluate colon damage. Plasma was obtained by aortic puncture and colonic mucosa was scraped off and the fatty acid pattern was determined by gas±liquid chromatography. Total, saturated, and monounsaturated plasma fatty acids were signi®cantly higher in both periods of ulcerative colitis as compared to controls. Plasma n-6 fatty acids were increased after treatment, but no signi®cant change s were observed concerning to n-3 fatty acids. With regard to colon mucosa, saturated and monounsaturated fatty acids did not change because of the disease; however, n-6 fatty acids decreased in the ®rst week and increased in the second week and n-3 fatty acids were increased. Changes on the fatty acid distribution in plasma did not parallel to those of colonic mucosa except for 22:6(n-3). We have also found that experimental ulcerative colitis induce d by trinitrobe nzene sulfonic acid reproduce s many of the features related to changes in plasma and colon mucosa fatty acids observed in the human disease. KEY WORDS: colon; fatty acid; in¯ammatory bowel disease; ulcerative colitis; trinitrobenzenesulfonic acid. Polyunsaturate d fatty acids (PUFA) as a key compo- nent in membrane function (1, 2) and precursors of eicosanoids (3± 6) play an important role in the patho- genesis of in¯ammatory bowel disease (IBD). As part of the cell membrane structure, PUFA modulate membrane enzyme and receptor activities by chang- ing membrane ¯uidity (1, 7). In addition, some arachidonic acid-derived eicosanoids, namely pros- taglandin E 2 (PGE 2 ), leukotriene B 4 (LTB 4 ), and thromboxane A 2 (TxA 2 ), have been involved in the pathoge nesis of IBD, on the basis of their increased concentrations in the in¯amed intestinal mucosa in the acute phase of the disease (8±13). The four different long-chain PUFA series share the same desaturase s and elongase s for their synthesis (14, 15), although their af®nities for these enzymatic systems are different. In addition, the components of the different fatty acid series are not interconvertible in vivo (14). These properties have made it possible to Manuscript received Decembe r 23, 1997; acce pted May 20, 1998. From the Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Granada, Spain. Address for reprint requests: Prof. Angel Gil, Department of Biochemistry and Molecular Biology, School of Pharmacy, Univer- sity of Granada, Campus Universitario de Cartuja, 18071 Granada, Spain. Digestive Diseases and Sciences, Vol. 43, No. 12 (December 1998), pp. 2688±2695 2688 Digestive Diseases and Sciences, Vol. 43, No. 12 (December 1998) 0163-2116/98/1200-2688$15.00/0 Ñ 1998 Plenum Publishing Corporation