Objective: Oxidative stress is suggested to play key role in the pathogenesis of inflammatory bowel diseases. Protein oxidation resulting from oxidative damage is notified in ulcerative colitis which is the one of the inflammatory bowel diseases. The aim of the study was to determine if N-acetylcysteine (NAC) was effective on protein oxidation resulting from ulcerative colitis.

Materials and Methods: During work, 40 male Wistar rats weighing 200 to 250 g were divided randomly into four groups: control (n=10), colitis (n=10), NAC₁ treatment (n=10) and NAC₂ treatment (n=10). 1 ml acetic acid (pH 2.4, 4%) was administered by intrarectal route to colitis and NAC treatment groups, whereas serum physiologically was administered to control group. N-acetylcysteine was injected to NAC₁ group (100 mg/kg) and NAC₂ group (500 mg/kg) intraperitoneally, while colitis and control groups were injected with serum physiologically (pH 7, %0.9 sodium chloride) at 24th hours after the acetic acid administration. In whole blood samples; whole blood glutathione, plasma thiol, nitrotyrosine, colon tissue samples total thiol, non-protein thiol, protein thiol, and advanced oxidation protein products were measured.

Results: Advanced oxidation protein products in colonic tissues, and plasma nitrotyrosine levels of colitis group were elevated in comparison with control group (both; p<0.01). A decrease was observed colonic tissue total-SH levels of colitis group as compared with control group (p<0.01). In NAC₁ group administration of N-acetylcysteine decreased the advanced oxidation protein products levels compared to control and colitis groups. (p<0.05, p<0.001; respectively).

Conclusion: As a result, administration of N-acetylcysteine partially prevents colonic tissue protein oxidation results from ulcerative colitis.