Abstract
In the present study, we examined the gastroprotective effect of selenium against ethanol-induced gastric mucosal lesions in rats. The gastric mucosal lesions were produced by oral administration with various concentrations of ethanol for three days, and 80% ethanol treatment was determined to be the optimal condition for induction of gastric damage. To identify the protective effect of selenium on ethanol-induced gastric damage, various doses of selenium were given as pretreatment for three days, and then gastric damage was induced by 80% ethanol treatment. Selenium showed a protective effect against ethanol-induced gastric mucosal lesions in a dose dependent manner. Specifically, 100 μg/kg selenium showed the highest level of gastroprotection. In addition, selenium markedly attenuated ethanol-induced lipid peroxidation in gastric mucosa and increased activities of radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase in a dose-dependent manner. Histological data showed that 100 μg/kg selenium distinctly reduced the depth and severity of the ethanol induced gastric lesion. These results clearly demonstrate that selenium inhibits the formation of ethanol-induced gastric mucosal lesions through prevention of lipid peroxidation and activation of enzymatic radical scavenging.
Highlights
The gastric mucosa is one of the most important tissues in an organism, because of its function, structure, and the pathological processes that can take place in this tissue [1,2]
Gastric mucosal lesions in rats were induced by ethanol, and the lesions produced were studied for identification of the gastroprotective effect of selenium
To demonstrate whether selenium affects the activity of radical scavenging enzymes involved in gastroprotection, the activity of glutathione peroxidase in the gastric mucosa of rats was determined by a modified method of Lawrence and Burk [33]
Summary
The gastric mucosa is one of the most important tissues in an organism, because of its function, structure, and the pathological processes that can take place in this tissue [1,2]. The oral administration of ethanol rapidly induces gastric mucosal lesions, and these ethanol-induced lesions are commonly used to study both the pathogenesis and therapy of human ulcerative disease [17,18,19]. An essential dietary element for mammals, has important metabolic functions in animals, including protection of membrane lipids and macromolecules from oxidative damage produced by peroxides [20], and activation of important antioxidant proteins, thioredoxin reductase and several selenoproteins [21,22]. This study was designed to investigate the gastroprotective effect of selenium by measuring the amount of lipid peroxidation and by comparing the activities of enzymatic scavengers, such as SOD, catalase and glutathione peroxidase
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