The crucial role of Se-dependent glutathione peroxidase (GP) in protection of the epithelial layer of gastrointestinal tract (GIT) mucosa from adverse effects of lipid peroxidation products is generally recognized. In its turn, GP biosynthesis depends on selenium (Se) allowances of the body. In studying a Se substance, the main goal was to assess its protective and antioxidative properties. The efficiency of selenomethionine (Se-Met) application to correct disturbances resulting from acute alcohol intoxication (AAI) was tested. The experiment was carried out on male albino adult Wistar CRL:(WI)WUBR rats. Four groups of the animals were involved in the study. Rats from Groups 3 and 4 were treated intragastrically with a SeMet solution (50 μg Se/kg body weight/day). Rats from Groups 1 (control) and 2 received water intragastrically. On day 11, Group 2 and 4 animals were treated intragastrically with a 25% ethanol solution (5g/kg body weight) for 2h, whereas Group 1 and 2 rats received an isovolume amount of water. The AAI-resulting OS was confirmed by significantly increased levels of blood thiobarbiturate-reacting products (TBARS) and corticosterone (CS). In this situation, the contents of reduced glutathione in duodenal (–24.4%), and the small intestinal mucosa (–14.1%), blood plasma (–15.6%) and erythrocytes (–19.3%) were decreased significantly. OS inhibited GP activity with H₂0₂ as substrate, which was particularly marked in gastric (–53.4%), duodenal (–24.4%) and rectal (–17%) mucosa. The activity of GP with t-BOOH as substrate was decreased (–41.4%) only in small intestinal mucosa. In its turn, the SeMet treatment prior to OS significantly reduced blood TBARS and OS levels and raised the activity of blood plasma and erythrocyte GP activity. Unchanging GP activity (H₂0₂) in the upper GIS regions, the SeMet supplementation prior to AAI activated the enzyme in rectal enterocytes, whereas GP with t-BOOH as substrate was activated in all the GIS regions, except for the small intestine. Thus, the saturation of the rat body with SeMet administered prior to AAI contributed to prevention of nearly all the negative alterations occurring in the glutathione system, GP functions and animal glucocorticosteroid status.

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