Change of energy supply oxidation indices changes in rats with type 2 diabetes mellitus and acetaminophen toxic lesions

Medical and Clinical Chemistry ◽

10.11603/mcch.2410-681x.2017.v0.i3.8194 ◽

2017 ◽

Author(s):

O. B. Furka

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Energy Supply ◽

Intraperitoneal Administration ◽

Liver Homogenate ◽

Intragastric Administration ◽

Starch Solution ◽

Citrate Buffer

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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Зміна деяких показників антиоксидантної системи в щурів з токсичним ураженням ацетамінофеном на тлі цукрового діабету 2 типу

Medical and Clinical Chemistry ◽

10.11603/mcch.2410-681x.2017.v0.i1.7688 ◽

2017 ◽

Author(s):

O. B. Furka ◽

I. B. Ivanusa ◽

M. M. Mykhalkiv ◽

I. M. Klishch

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Antioxidant System ◽

Intraperitoneal Administration ◽

Liver Homogenate ◽

Intragastric Administration ◽

Starch Solution ◽

Citrate Buffer

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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ACETAMINOPHEN EFFECT ON FREE RADICAL OXIDATION INDICES IN RATS WITH TYPE 2 DIABETES MELLITUS

International Journal of Medicine and Medical Research ◽

10.11603/ijmmr.2413-6077.2017.2.8372 ◽

2017 ◽

Author(s):

O. B. Furka ◽

I. B. Ivanusa ◽

M. M. Mykhalkiv ◽

I. M. Klishch

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Free Radical ◽

Liver Homogenate ◽

Free Radical Oxidation ◽

Maximum Increase ◽

Radical Oxidation ◽

Age Related

Background. Acetaminophen is a drug used to relieve pain syndrome. It is used both independently and in composition of combined drugs. Type 2 diabetes is an age-related disease that is associated with a violation of insulin synthesis by pancreas.Objective. The aim of the research was to study the effect of acetaminophen on major free radical oxidation indices of rats with type 2 diabetes mellitus in time dynamics.Methods. We conducted two series of experiments. The first series comprised rats with type 2 diabetes mellitus and acute acetaminophen toxic lesions. The second series involved rats with type 2 diabetes mellitus and acetaminophen administration at a dose of 55 mg/kg for the period of 7 days.Results. Administration of acetaminophen for rats with type 2 diabetes mellitus caused the increase in the content of malondialdehyde, diene and triene conjugates and Schiff bases in blood plasma and malondialdehyde, diene and triene conjugates in liver homogenate. The maximum increase in these indices was observed on the first day of the experiment. Gradually these indices decreased on the 3rd, 5th and 7th days of the experiment.Conclusions. Free radical oxidation increased in both series of the experiment. This process developed in rats with type 2 diabetes mellitus and acute acetaminophen toxic lesions more intensively, than in rats with type 2 diabetes mellitus and administration of acetaminophen at the highest therapeutic dose during 7 days.

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APOPTOTIC PROCESSES’ RESEARCH ON THE MODEL OF TYPE 2 DIABETES MELLITUS ON OBESITY’S BACKGROUND UNDER THE INFLUENCE OF DENSE BEAN EXTRACT

Wiadomości Lekarskie ◽

10.36740/wlek202008119 ◽

2020 ◽

Vol 73 (8) ◽

pp. 1690-1695

Author(s):

Viktoria A. Rybak ◽

Viktoria V. Korol ◽

Natalia V. Derkach

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Cell Function ◽

Male Rats ◽

Control Group ◽

Citrate Buffer ◽

Pancreatic Cell ◽

Alcoholic Fatty Liver

The aim of the study was to observe the influence of dense bean extract on the intensity of apoptotic processes in the liver cells and pancreas of rats on a model of type 2 diabetes mellitus on obesity’s background. Materials and methods: The main method was to model type 2 diabetes mellitus on the background of obesity in organism of mature six-month-old male rats of the Wistar population (n = 21), weighing 150-170 g. The modelling was carried out by intraperitoneal low dose administration of streptozotocin (30 mg / kg, in citrate buffer pH = 4, 5) inside after three months period of keeping animals on a combined diet. Apoptosis in DNA samples of liver and pancreas cells was identified in duplicates using electrophoresis in a 1% agarose gel with using a 1kb DNA SibEnzyme apoptosis marker (from 10,000 to 250 nucleotides). Results: Only in two of the seven studied DNA samples of the pancreas of a group of rats, treated with a dense bean extract, were observed the traces of necrosis without detectable manifestations of the apoptotic process. It situates at the level of indicators of the animals’ intact control group and indicates the distinct effect’s presence which includes maintaining pancreas cells survival (in both endocrine and exocrine parts) if imbalance of carbohydrate and lipid metabolism take place in organism. Conclusion: Dense bean extract showed a more distinct effect than the comparison drug metformin in relation to the risk of premature loss of pancreatic cell function and the development of non-alcoholic fatty liver disease. A dense bean extract is promising for further pharmacological studies, with the aim of creating phytopreparations – «Glyphasonorm» tablets and «Glyfasolin» capsules for the correction of type 2 diabetes mellitus and its complications.

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

Medical and Clinical Chemistry ◽

10.11603/mcch.2410-681x.2017.v0.i2.8946 ◽

2018 ◽

Author(s):

O. B. Furka

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Body Weight ◽

Antioxidant System ◽

The Body ◽

Intraventricular Injection ◽

Control Group ◽

Starch Solution

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.

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Metabolic and Cognitive Effects of Ranolazine in Type 2 Diabetes Mellitus: Data from an in vivo Model

Nutrients ◽

10.3390/nu12020382 ◽

2020 ◽

Vol 12 (2) ◽

pp. 382 ◽

Cited By ~ 2

Author(s):

Velia Cassano ◽

Antonio Leo ◽

Martina Tallarico ◽

Valentina Nesci ◽

Antonio Cimellaro ◽

...

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Body Mass ◽

Mass Composition ◽

In Vivo Model ◽

Control Group ◽

Long Term Memory ◽

Citrate Buffer

Type 2 diabetes mellitus (T2DM) is a risk factor for cognitive impairment. Ranolazine, an anti-ischemic drug used in the treatment of angina pectoris, has been shown to possess hypoglycemic properties in pre-clinical and clinical studies. The aim of this study was to evaluate the effects of ranolazine on glucose metabolism and cognitive function in a T2DM model of Wistar rats. Diabetes was induced by a high fat diet (HFD) and streptozotocin (STZ). The control group received a normal caloric diet (NCD) and sodium citrate buffer. Metformin, an effective hypoglycemic drug, was employed as a positive control. Animals were divided into the following groups: HFD/STZ + Ranolazine, HFD/STZ + Metformin, HFD/STZ + Vehicle, NCD + Vehicle, NCD + Ranolazine, and NCD + Metformin. Rats received ranolazine (20 mg/kg), metformin (300 mg/kg), or water, for 8 weeks. At the end of the treatments, all animals underwent to an intraperitoneal glucose tolerance test (IPGTT) and behavioral tests, including passive avoidance, novel object recognition, forced swimming, and elevate plus maze tests. Interleukin-6 plasma levels in the six treatment groups were assessed by Elisa assay. Body mass composition was estimated by nuclear magnetic resonance (NMR). Glucose responsiveness significantly improved in the HFD/STZ + Ranolazine (p < 0.0001) and HFD/STZ + Metformin (p = 0.003) groups. There was a moderate effect on blood glucose levels in the NCD + Ranolazine and NCD + Metformin groups. Lean body mass was significantly increased in the HFD/STZ + Ranolazine and HFD/STZ + Metformin animals, compared to HFD/STZ + Vehicle animals. Ranolazine improved learning and long-term memory in HFD/STZ + Ranolazine compared to HFD/STZ + Vehicle (p < 0.001) and ameliorated the pro-inflammatory profile of diabetic mice. These results support the hypothesis of a protective effect of ranolazine against cognitive decline caused by T2DM.

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