OXIDATIVE STRESS IN GASTRIC MUCOSA IN EXPERIMENTAL MODELS OF ACUTE ULCEROGENESIS. EFFECT OF PARACETAMOL AND PROPACETAMOL

The role of the oxidative stress in acute experimental ulcerogenesis with different pathogenesis and the effect of paracetamol and propacetamol were investigated. The study was performed on male Wistar rats (220-250g) body weight. Gastric ulcer was induced by cold restraint stress (CRS, 4 hours, 4°C), acetyl salicylic acid (ASA, 300mg/kg, 0,2mL/100 g b. w., p. o.) and absolute ethanol (1 ni 1. animal, p. o.). For the assessment of the ulcerogenesis a mean ulcer area and as markers for the oxidative stress malon dialdehyde (MDA), reduced glutathione (GSH) and uric acid (UA) levels in mucosa were used. The mean ulcer area was 101,4, 13,6 and 9,31mm2 for ethanol, CRS and ASA models. Lipid peroxidation evaluated as MDA level was activated strongly in CRS and ASA and mildly in ethanol-induced ulcerogenesis. The GSH was significantly higher in CRS and ASA models. Paracetamol (250mg/kg) and propacetamol (500mg/kg) exerted antiulcerogenic effect in the three experimental models, more pronounced for paracetamol. Their protective effect was strongest (68% and 85%, respectively) for absolute ethanol. Paracetamol and propacetamol decreased MDA in gastric mucosa and sustained the elevated levels of GSH and uric acid. Gastric ulcer induced by CRS, ASA and absolute ethanol was associated with activation of lipid peroxidation. Paracetamol and propacetamol showed gastroprotective effect associated with decreased lipid peroxidation in gastric mucosa