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Articles by Mustafa ZERIN
Total Records ( 1 ) for Mustafa ZERIN
  Mustafa ZERIN , Ali Ziya KARAKILCIK , Muharrem BITIREN , Davut MUSA , Abdullah OZGONUL , Sehabettin SELEK , Yasar NAZLIGUL and Ali UZUNKOY
  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 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.
 
 
 
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