摘要
AIM: To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats. METHODS: Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control. At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples. RESULTS: Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P < 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples. CONCLUSION: Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.
AIM： To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats. METHODS： Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L （low dose） or 5000 mg/L （high dose） of lead acetate for 15 wk. A third group received saline and served as control. At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples. RESULTS： Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively （P 〈 0.0）. On the other hand, lead exposure significantly decreased catalase and superoxide dismutase （SOD） activities and the amount of nitrite in gastric mucosal samples. CONCLUSION： Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.
基金
Supported by the Senate, University of Ibadan, Nigeria partly through SRG grant to SBO UI/SRG/COM/2000/10A
