Change of energy supply oxidation indices changes in rats with type 2 diabetes mellitus and acetaminophen toxic lesions
Keywords:acetaminophen, cytochrome oxidase, succinate dehydrogenase, diabetes mellitus.
Introduction. Acetaminophen is an effective and safe drug for emergency usage, but there are contraindications for its usage. Diabetes mellitus is an endocrine disease, which caused by the absolute or relative deficiency of pancreas hormone (insulin).
The aim of the study – to learn the change of energy supply oxidation indices in animals with type 2 diabetes mellitus and acetaminophen toxic lesions in time dynamics.
Research Methods. We conducted two series of experiments. In the first series toxic lesion was caused by a single intragastric administration of acetaminophen suspension in 2 % starch solution to animals in a dose of 1250 mg/kg (1/2 LD50). In the second series the suspension of acetaminophen in 2 % starch solution in a dose of 55 mg/kg was given. Non-genetic form of experimental type 2 diabetes mellitus was modeled by a single intraperitoneal administration of streptozotocin solution in doses 65 mg/kg, which was diluted by citrate buffer (pH 4.5) with the previous intraperitoneal nicotinamide administration in doses of 230 mg/kg. Rats, which were given the same amount of solvent (citrate buffer pH 4.5), were used as the control group.
Results and Discussion. Cytochrome oxidase and succinate dehydrogenase activity decreased in rat liver homogenate under the influence of acetaminophen with type 2 diabetes mellitus throughout the experiment.
Conclusions. Acetaminophen administration to rats with type 2 diabetes mellitus causes significant violations of energy supply oxidation.
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