Vitamin C modulates oxidative stress-induced colitis in rats

Aim: 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 andintestinal 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, theydecreased 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 inpreventing oxidative stress and colonic tissue injury produced by acetic acid.