Вплив ураження ацетамінофеном на тлі цукрового діабету типу 2 на зміни показників глутатіонової системи

Abstract

Introduction. The most important function of the liver in the body is neutralization and destruction of toxic substances. Metabolism and utilization of chemical and biological toxins are carried out by neutralizing the hepatocyte system, followed by the removal of harmful products from the body.The aim of the study – to investigate the effect of acetaminophen on the background of type 2 diabetes mellitus on the main parameters of the glutathione unit of the antioxidant system in rat liver homogenate in time dynamics.Research Methods. The experiments were carried out on white mature rats weighing 180–220 g, contained on a standard ration of the vivarium and free access to water. We conducted 2 series of experiments. In the first, toxic acetaminophen was caused by a single intraventricular injection of acetaminophen in 2 % starch solution at a dose of 1250 mg/kg body weight (1/2 LD50), in the second suspension of acetaminophen in a 2 % starch solution at a dose of 55 mg/kg, which corresponds to the highest therapeutic dose for 7 days. The non-genetic form of experimental type 2 diabetes mellitus was modeled according to the method of Islam S., Choi H. (2007) by a single intraperitoneal injection of a streptozotocin solution (“Sigma”, USA) at a body weight (200±20) g at a rate of 65 mg/kg, which diluted with citrated buffer (pH 4.5) with a preliminary (within 15 minutes) intraperitoneal administration of nicotinamide in a dose of 230 mg/kg. For the control group, rats with the same body weight were administered with a similar volume of solvent (citrate buffer pH 4.5).Results and discussion. Activation of lipid peroximation reactions is one of the fundamental biological mechanisms of damage to biostructures and the development of cellular pathology for the actions of damaging factors of various genesis, especially under the conditions of xenobiotics.Conclusion. Acetaminophen poisoning against type 2 diabetes mellitus causes a significant disruption of compensatory mechanisms, especially the state of the enzyme and non-enzyme links of the antioxidant system.