Furka O. Oxidative status and antioxidant protection state of rats with type 2 diabetes mellitus and acetaminophen toxic lesions

It was investigated the features of the oxidative status and antioxidant protection state of state of rats with type 2 diabetes mellitus and acetaminophen toxic lesions. It was determined, that acute poisoning by acetaminophen animals with type 2 diabetes caused more visible activation of microsomal oxidation in the postmithohondrial fraction of the liver and free radical oxidation of lipids and proteins in the blood and liver of rats than in normal glycemic animals. Activity of superoxide dismutase and catalase in plasma of blood and liver tissue, and glutathione system decreased, which is indicated on inhibition of the antioxidant system; concentration of ceruloplasmin decreased compared to normal glycemic animals with acetaminophen administration. Type 2 diabetes mellitus caused significant violations of energy supply oxidation processes at a single administration of acetaminophen (1/2 LD50), which suggests a succinate dehydrogenase and cytochrome oxidase activity decrease in the liver tissue compared to normal glycemic animals, which were modeled acute poisoning by acetaminophen. Also, it was observed violation of hepatocytes membranes integrity with the release of intracellular enzymes – ALAT, ASAT, in animals with type 2 diabetes and acute acetaminophen poisoning significantly higher in comparison to animals with only acetaminophen lesion. Similar results were obtained at seven-days administration of the drug at a higher therapeutic dose, however, but less pronounced than acute lesions.