Changes of some indices of antioxidant system in rats with type 2 diabetes mellitus and acetaminophen toxic lesions
DOI:
https://doi.org/10.11603/mcch.2410-681X.2017.v0.i1.7688Keywords:
acetaminophen, ceruloplasmin, catalase, superoxide dismutase, peroxidase activity of blood, diabetes mellitus.Abstract
Introduction. Acetaminophen has dose-dependent effect on the liver, which is the degree of damage depends on the concentration of this drug in plasma. When administration in large quantities of acetaminophen (accidentally or with suicidal intent) centrolobular massive necrosis occurs in the liver. Diabetes is also a risk factor for cirrhosis.
The aim of the study – to study the effect of acetaminophen on main indices of antioxidant system in liver homogenate and blood plasma of rats with type 2 diabetes mellitus in time dynamics.
Methods of the research. 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, which corresponds to the highest therapeutic dose during 7 days. Non-genetic form of experimental type 2 diabetes mellitus was modeled by single intraperitoneal administration of streptozotocin solution in doses 65 mg/kg to rats, which was diluted by citrate buffer (pH 4.5) with the previous intraperitoneal nicotinamide administration in doses of 230 mg/kg. Rats with the same body weight, which were given the same amount of solvent (citrate buffer pH 4.5), were used as the control group.
Results and Discussion. The results of the experiment show that a greater toxicity in the experimental animals causes the administration of acetaminophen on the background of type 2 diabetes.
Conclusion. Toxic lesion by acetaminophen in rats with type 2 diabetes mellitus is accompanied by significant violation of enzymatic components of the antioxidant system, have a compensatory nature and direct to neutralize of free radical oxidation products.
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