| الوصف: |
Objective: to assess the pathological significance of a lipid peroxidation (LPO) process after severe intoxications caused by organophosphorous compounds, alcohol, dichloroethane, the efficiency of its correction with the antioxidants pyrimi-dine and benzimidazole derivatives. Materials and methods. The study was conducted on male rats weighing 160—230 g. Models of intoxications with ethanol, dichloroethane, carbofos, armine, or sodium nitrite in the doses causing 30—50% death were employed. LPO products were studied in the lipid extracts of the brain, myocardium, and liver by various methods. The activity of a number of enzymes (catalase, glucose-6-phosphate dehydrogenase, superoxide dismutase, glutathione peroxidase, Na+, K+-ATPase) was evaluated in the rats. Serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, alkaline phosphatase, and acid phosphotase were spectrophotometrically assayed. Quantitative histochemistry was used to determine the activity of succinate dehydrogenase, NAD-diaphorase, and Na+, K+-ATPase. The number of chemical reactions was measured and estimated on a MT-9 TV analyzer microscope. Experimental findings were analyzed by different variation statistical methods using Student’s test. Results. The paper reports the results of comprehensive experimental studies of the efficiency of correction of prooxidative-antioxidative imbalance after severe acute intoxication with chemical prooxidants and some lipophilic xenobiotics. Antioxidants, anti-hypoxants, and actoprotectors, the derivatives of pyrimidine and benzimidazole, were tested. Conclusion. The findings suggest that the immediate sequels of prooxidative-antioxidative imbalance due to experimental intoxications with ethanol, dichloroethane, and organophosphorous compounds are impaired activities of LPO processes, oxidative stress, altered metabolic, bioenergetic processes in organs and tissues. The use hydroxymethyluracil, bemitil, or thietazole largely limits or prevents the above disorders. |
