scholarly journals THE RATIO OF SYSTEMIC INFLAMMATION, OXIDATIVE STRESS AND GLUTATHIONE REDOX STATUS INDICATORS IN PATIENTS WITH CORONARY HEART DISEASE AND TYPE 2 DIABETES MELLITUS

2013 ◽  
Vol 19 (4) ◽  
pp. 356-366
Author(s):  
A. G. Moiseenok ◽  
I. V. Buko ◽  
I. V. Gorudko ◽  
E. E. Konstantinova ◽  
N. L. Tsapaeva ◽  
...  

Objective. To study and compare indicators of systemic inlammation and red blood cells glutathione redox potential by chronic oxidative stress (OS) in patients with coronary heart disease (CHD), type 2 diabetes mellitus (T2DM) and the combination of both diseases.Design and methods. The study included 35 patients with CHD and newly diagnosed T2DM, 109 patients with CHD, 19 patients with T2DM, and 89 healthy individuals. Systemic inlammation indicators were measured including concentration of interleukin (IL) 6 and 8, myeloperoxidase (MPO) and OS in plasma, oxidized (GSSG) and reduced (GSH) glutathione, as well as their ratio and redox potential (E), the activity of glutathione reductase (GR) and glutathione peroxidase (GP) in red blood cells.Results. Signiicant growth of systemic inlammation (IL-6, IL-8, MPO) indicators on the weakening antioxidant defense enzyme has been registered in patients with a combination of CHD and T2DM, a 3,4-fold reduction of GSH level, 5,8-fold of 2GSH/GSSH in red blood cells and E values towards the oxidized state at 36,3 mV were noted. These changes were less pronounced in CHD group and were absent in T2DM group. All subjects showed a decreased activity of GP and increased level of glycosylated hemoglobin. The correlation of E and activity GR have been found in patients with carbohydrate metabolism disorder. High positive relationship between IL concentration and red blood cells GR, E indicators has been identiied in patients with CHD and T2DM. There is a need to control and correct cellular redox potential in patients with CHD and T2DM.Conclusion. The combination of CHD and T2DM contributes to the decrease of red blood cells redox status glutathione secondary to the increased systemic inlammatory response and chronic OS indicators.

2013 ◽  
Vol 53 (3) ◽  
pp. 239-245 ◽  
Author(s):  
Ebrahim Mostafavi ◽  
Manouchehr Nakhjavani ◽  
Zaniar Ghazizadeh ◽  
Hassan Barakati ◽  
Hossein Mirmiranpour ◽  
...  

2020 ◽  
Vol 119 (5) ◽  
pp. 900-912
Author(s):  
Yixiang Deng ◽  
Dimitrios P. Papageorgiou ◽  
Xuejin Li ◽  
Nikolaos Perakakis ◽  
Christos S. Mantzoros ◽  
...  

Redox Report ◽  
2008 ◽  
Vol 13 (6) ◽  
pp. 277-282 ◽  
Author(s):  
Stephney Whillier ◽  
Julia Elizabeth Raftos ◽  
Philip William Kuchel

2017 ◽  
Vol 113 (2) ◽  
pp. 481-490 ◽  
Author(s):  
Hung-Yu Chang ◽  
Xuejin Li ◽  
George Em Karniadakis

2020 ◽  
Vol 25 (5) ◽  
pp. 29-35
Author(s):  
M. Yu. Maksimova ◽  
A. V. Ivanov ◽  
K. A. Nikiforova ◽  
F. R. Ochtova ◽  
E. T. Suanova ◽  
...  

Ischemic stroke (IS) and type 2 diabetes mellitus are factors that affect the homeostasis of low-molecularweight aminothiols (cysteine, homocysteine, glutathione etc.). It has already been shown that IS in the acute period led to a decrease a level of reduced forms of aminothiols, but it is not clear whether type 2 diabetes mellitus has a noticeable effect there. Objective: to reveal the features of homeostasis of aminothiols in patients with type 2 diabetes mellitus in acute IS. Material and methods. The study involved 76 patients with primary middle cerebral artery IS in the first 10–24 hours after development of neurological symptoms. Group 1 included 15 patients with IS and type 2 diabetes mellitus, group 2 — 61 patients with IS and stress hyperglycemia. Their total plasma levels of cysteine, homocysteine, and glutathione, their reduced forms, and redox status were determined at admission (in the first 24 hours after IS). Results. There was a decrease in the level of total glutathione level (1.27 vs. 1.65 μM, p = 0.021), as well as its reduced form (0.03 vs. 0.04 μM, p = 0.007) in patients with IS and type 2 diabetes mellitus. Patients with type 2 diabetes mellitus who had a low redox status of homocysteine (0.65–1.2%) and glutathione (0.7–2.0%) were also characterized by a decrease in total glutathione level (p = 0.02; p = 0.03). Conclusion. Thus, type 2 diabetes mellitus is associated with a decrease in the level of total glutathione in acute IS. Probably, type 2 diabetes mellitus is characterized by a particular relationship between the metabolism of homocysteine, glutathione and glucose. Therefore, the search for homocysteine-dependent approaches to correct glutathione metabolism in type 2 diabetes mellitus may be of interest as an adjuvant therapy for IS.


2020 ◽  
Vol 26 ◽  
Author(s):  
Margarita A. Sazonova ◽  
Anastasia I. Ryzhkova ◽  
Vasily V. Sinyov ◽  
Marina D. Sazonova ◽  
Tatiana V. Kirichenko ◽  
...  

Background: The present review article considers some chronic diseases of vascular and metabolic genesis, the causes of which may be mitochondrial dysfunction. Very often, in the long course of the disease, complications may occur, leading to myocardial infarction or ischemic stroke and as a result, death.In particular, a large percentage of human deaths nowadays belongs to cardiovascular diseases such as coronary heart disease (CHD), arterial hypertension, cardiomyopathies and type 2 diabetes mellitus. Objective: The aim of the present review was the analysis of literature sources, devoted to an investigation of a link of mitochondrial DNA mutations with chronic diseases of vascular and metabolic genesis, Results: The analysis of literature indicates the association of the mitochondrial genome mutations with coronary heart disease, type 2 diabetes mellitus, hypertension and various types of cardiomyopathies. Conclusion: The detected mutations can be used to analyze the predisposition to chronic diseases of vascular and metabolic genesis. They can also be used to create molecular-cell models necessary to evaluate the effectiveness of drugs developed for treatment of these pathologies. MtDNA mutations associated withthe absence of diseases of vascular and metabolic genesis could be potential candidates for gene therapy of diseases of vascular and metabolic genesis.


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