Ali UZUNKÖY, Davut MUSA, Abdullah ÖZGÖNÜL, Şehabettin SELEK, Muharrem BİTİREN, Yaşar NAZLIGÜL, Mustafa ZERİN, Ali Ziya KARAKILÇIK

Vitamin C modulates oxidative stress-induced colitis in rats

Free radicals are an important factor in the etiopathogenesis of colitis and may increase oxidative damage. The antioxidant vitamin C efficiently scavenges free oxygen radicals. The present study aimed to investigate the probable protective effects of vitamin C on oxidative injury in rats in which colitis was experimentally induced with acetic acid. Materials and methods: This study was conducted with rats for a period of 7 days. Group 1 intrarectally received a placebo (0.9% NaCl) and group 2 intrarectally received 2 mL of 5% acetic acid (AA) and the placebo. Group 3 intrarectally received 2 mL of 5% AA and vitamin C (100 mg/kg of body weight) via gastric gavage. Myeloperoxidase (MPO), catalase (CAT), prolidase (PRS), and arylesterase (ARE) activity, and total thiol (T-SH), total antioxidant capacity (TAC), total oxidant status (TOS), lipid hydroperoxide (LOOH), and oxidative stress index (OSI) values were analyzed in blood and intestinal samples. Results: While CAT and PRS activity, and plasma TOS, LOOH, and OSI increased following the administration of AA, TAC decreased. TAC increased, whereas LOOH and OSI decreased in response to vitamin C treatment. While MPO and CAT activity, and TOS, LOOH, and OSI values in the colon increased in response to AA treatment, PRS, ARE, T-SH, and TAC decreased. TAC increased in response to vitamin C, whereas MPO, PRS and ARE activity, and TOS, LOOH, and OSI values decreased. While histopathologic colonic injury scores increased (P < 0.001) in response to AA, they decreased in response to vitamin C. Conclusion: Histopathological damage scores, MPO, TOS, LOOH, and OSI decreased significantly in response to vitamin C treatment, whereas TAC increased. Based on these results, we think that vitamin C might play an important role in preventing oxidative stress and colonic tissue injury produced by acetic acid.

Anahtar Kelimeler:

Key words: Vitamin C, colitis, histopathology, oxidative stress, rats

Vitamin C modulates oxidative stress-induced colitis in rats

Keywords:

Key words: Vitamin C, colitis, histopathology, oxidative stress, rats,

PDF

___

Keshavarzian A, Morgan G, Sedghi S, Gordon JH and Doria M. Role of reactive oxygen metabolites in experimental colitis. Gut 1990; 31; 786-90. 2. Millar A D, Rampton DS, Chander CL, Claxson AW, Blades S, Coumbe A et al. Evaluating the antioxidant potential of new treatments for inflammatory bowel disease using a rat model of colitis. Gut 1996; 39: 407-15. 3. Pravda J. Radical induction theory of ulcerative colitis. World J Gastroenterol 2005; 11: 2371-84
Fiocchi C. Inflammatory bowel disease: Aetiology and pathogenesis. Gastroenterology 1998; 115: 182–205.
Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuk MR and Wallace JL. Hapten-induced model of chronic inflammation and ulceration in the rat colon. Gastroenterology 1989; 96:795–803.
Goth L. A simple method for determination of serum catalase activity and revision of reference range. Clin Chim Acta 1991; 196: 143–152.
Kelly G. The interaction of cigarette smoking and antioxidants. Part III: Ascorbic acid. Altern Med Rev 2003; 8:43–54.
Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem 2005; 38: 1103-11.
Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem 2004; 37: 112-119.
Myara I, Charpentier C, Lemonnier A. Optimal conditions for prolidase assay by proline colorimetric determination: Application to iminodipeptiduria. Clin Chim Acta 1982; 125:193-205.
Aslan M, Kosecik M, Horoz M, Selek S, Celik H, Erel O. Assessment of paraoxonase and arylesterase activities in patients with iron deficiency anemia. Atherosclerosis 2007; 191: 397-402.
Krawisz JE, Sharon P, Stenson WF. Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity: Assessment of inflammation in rat and hamster models. Gastroenterology 1984; 87:1344-50.
Lih-Brody L, Powell SR, CollierKP, Reddy GM, Cerchia R, Kahn E et al. Increased oxidative stress and decreased antioxidant defenses in mucosa of inflammatory bowel disease. Dig Dis Sci 1996; 41: 2078–86.
Mansour MA, Nagi MN, El-Katip AS, Al_Bekairi AM. Effect of tymoquinone on antiioxidant enzyme activities lipid peroxidation and DT-diaphorase in different tissues of mice: a possible mechanism of action. Cell Biochem and Funct 2002; 20, 143-151.
Hogan JS, Smıth KL, Weıss WP, Todhunter DA and Schockey WL. Relationships among vitamin E, Se and bovine blood neutrophils. J Dairy Sci 1990; 73: 2372-78.
Memişoğulları R, Gumuştekın K, Dane Ş, Akcay F. The effect of pre-ınjury supplementation with selenium or vitamin e on lipid peroxidation and antioxidant enzymes in burn ınjury. Turk J Med Sci 2006; 36: 141-146.
Yıldırım ,A, Kotan D, Yıldırım S, Aygül R, Akçay F. Increased lipid peroxidation and decreased antioxidant response in serum and cerebrospinal fluid in acute ıschemic stroke. Turk J Med Sci 2007; 37: 75-81
Özgönül A, Aksoy N, Dilmeç F, Uzunköy A, Aksoy Ş. Measurement of total antioxidant response in colorectal cancer using a novel automated method. Turk J Med Sci 2009; 39: 503- 506.
Aslan M, Nazligul Y, Horoz M, Bolukbas C, Bolukbas F, Aksoy N et al. Serum prolidase activity and oxidative status in Helicobacter pylori infection. Clin Biochem 2007; 40: 37-40.
Ancha HR, Kurella RR, McKımmey CC, Lıghtfoot S, Harty RF. Luminal antioxidants enhance the effects of mesalamine in the treatment of chemically ınduced colitis in rats. Exp Biol Med 2008; 233: 1301-1308.
Bregano JW, Dichi JB, Barbosa DS, Zebian MK, Matsuo T, Rodrigues MA, Cecchini R, Dichi I. Decreased total antioxidant capacity in plasma, but not tissue, in experimental colitis. Dig Dis Sci 2009; 54:751-757.
Nıeto N, Torres MI, Fernandez MI, Gıron MD, Rıos A, Suarez MD et al. Experimental ulcerative colitis ımpairs antioxidant defense system in rat intestine. Dig Dis Sci 2000; 45: 1820-1827.
Kruidenier L, Kuiper I, Van Duijn W, Mieremet-Ooms MAC, Van Hogezand RA, Lamers CBHW et al. Imbalanced secondary mucosal antioxidant response in inflammatory bowel disease. J Pathol 2003; 201: 17–27.
Bitiren M, Karakilcik AZ, Zerin M, Ozardalı I, Selek S, Nazlıgül Y, et al. Protective effects of Se and vitamin E combination on experimental colitis in blood plasma and colon of rats. Biol Trace Elem Res 2009 Sep 23. [Epub ahead of print].
Reifen R, Nissenkorn A, Matas Z and Bujanover Y. 5-ASA and lycopene decrease the oxidative stress and inflammation induced by iron in rats with colitis. J Gastroenterol 2004; 39: 514-519.
Hajj Hussein IA, Tohme R, Barada K, Mostafa MH, Freund JN, Jurjus RA et al. Inflammatory bowel disease in rats: Bacterial and chemical interaction. World J Gastroenterol 2008; 14: 4028- 39.
Komarnisky LA, Christopherson RJ, Basu TK. Sulfur: its clinical and toxicologic aspects. Nutrition 2003; 19: 54-61.
McKeown MJ, Hall ND, Corvalan JR. Defective monocyte accessory function due to surface sulphydryl (SH) oxidation in rheumatoid arthritis. Clin Exp Immunol 1984; 56: 607-13.
Jarvik GP, Tsai NT, McKinstry LA, Wani R, Brophy VH., Richter RJ et al. Vitamin C and E intake is associated with increased paraoxonase activity. Arteioscler Thromb Vasc Biol 2002; 22: 1329-33.
Namiduru ES, Özdemir Y, Kutlar I, Ersoy Ü. A study of prolidase in mothers, their newborn babies and in non- pregnant controls. Arch Gynecol Obstet 2001; 265: 73-5.
Myara I, Myara A, Mangeot M, Fabre M, Charpentier C, Lemonnier A. Plasma prolidase activity: A possible index of collagen catabolism in chronic liver disease. Clin Chem 1984; 30: 211-15.
Sutherland WH, Walker RJ, De Jong SA, Van Rij AM, Phillips V, Walker HL. Reduced postprandial serum paraoxonase activity after a meal rich in used cooking fat. Arterioscler Thromb Vasc Biol 1999; 19: 1340-47.
Beynen AC, Weınans GJB, Katan MB. Arylesterase actıvıtıes ın the plasma of rats, rabbıts and humans on low- and high- cholesterol diets. Comp Biochem Physiol 1984; 78 : 669-673.