The Effect Of Sodium Selenite Treatment In An Experimental Model Of Acute Glyphosphate Poisoning

Background. The aim of this study was to investigate the possibility of using sodium selenite as a treatment for acute glyphosate poisoning using the activity of the lipid peroxidation and antioxidant defence systems as a readout for efficacy. Material and methods. Experimental glyphosate poisoning and subsequent treatment using sodium selenite was performed in albino rats (105). Glyphosate was given in doses of 50, 100 and 130 mg/kg, and sodium selenite was administered at a dose of 2 mu g/kg. The blood concentrations of lipid peroxidation markers including conjugates of diene andtrienoic and malondialdehyde were determined. The endogenous glutathione (reduced form) level and activities of catalase, superoxide dismutase and glutathione peroxidase in the serum were measured. Results. Glyphosate poisoning has been found to result in a significant increase in lipid peroxidation activity. For example, malonic dialdehyde demonstrates a 2.35 times increase at a glyphosate dose of 130 mg/kg. At the experimental glyphosate poisoning dose of 100 mg/ kg the measurements of superoxide dismutase and glutathione peroxidase have been found to decrease 1.58 and 2.21 times, respectively. At a dose of 130 mg/kg, those values decreased 2.51 and 4.76 times, respectively, compared to untreated controls. Conclusions. The use of sodium selenite at a dose of 2 mu g/kg after poisoning of white rats with glyphosate (at doses of 50, 100 and 130 mg/kg) normalizes the lipid peroxidation and antioxidant defence activities of the body.