[Markers of redox potential of blood leukocytes in acute coronary syndrome, depending on the presence of type 2 diabetes mellitus].

Aim      Evaluating the redox potential of white blood cells (WBC) in acute coronary syndrome (ACS) depending on the presence or absence of type 2 diabetes mellitus (DM2).Material and methods  The study included 100 men and women aged 35 to 65 years who were managed for ACS at the Primary Vascular Department (PVD) of the Vladivostok Clinical Hospital #1. The control group consisted of 30 healthy volunteers matched with ACS patients in major anthropometric characteristics. Examinations were performed according to clinical recommendations. Blood was withdrawn for measuring cell activity of enzymes (superoxide dismutase, SOD; succinate dehydrogenase, SDH; and glutathione reductase, GR) and serum concentration of malonic dialdehyde (MDA). Based on the ACS type, all patients were divided into 3 main ACS groups, and then the groups were subdivided into subgroups based on the presence of DM2.Results Development of ACS was associated with changes in WBC redox potential. These changes were characterized by a significant decrease in SDH activity in all ACS patients, irrespective of their ACS type, and a moderate decease in GR in patients with myocardial infarction compared to patients with unstable angina and healthy volunteers. At the same time, the SOD activity and MDA concentration were practically unchanged compared to the control group. There were practically no significant differences in the enzyme activities between the ACS subgroups with or without DM2.Conclusion      The WBC activities of SDH and GR on day 1 of ACS can be considered as the indicators for early diagnosis of mitochondrial dysfunction resulting from the cardiovascular catastrophe as well as the markers for impaired primary cell defense. MDA and SOD values are not informative for determining the intensity of oxidative stress and further damage of the antioxidant system.

[1]  A. Hasan,et al.  Elevated DNA Damage, Oxidative Stress, and Impaired Response Defense System Inflicted in Patients With Myocardial Infarction , 2018, Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis.

[2]  B. Stockwell,et al.  Lipid peroxidation in cell death. , 2017, Biochemical and biophysical research communications.

[3]  P. Pollard,et al.  Succinate: a new epigenetic hacker. , 2013, Cancer cell.

[4]  M. Broncel,et al.  Increased oxidative stress and decreased membrane fluidity in erythrocytes of CAD patients. , 2013, Biochemistry and cell biology = Biochimie et biologie cellulaire.

[5]  A. Parekh,et al.  The challenge of multiple comorbidity for the US health care system. , 2010, JAMA.

[6]  P. Pasupathi,et al.  Free radicals and antioxidant status in acute myocardial infarction patients with and without diabetes mellitus. , 2010, Bangladesh Medical Research Council bulletin.

[7]  P. Puddu,et al.  The emerging role of cardiovascular risk factor-induced mitochondrial dysfunction in atherogenesis , 2009, Journal of Biomedical Science.

[8]  N. Weintraub,et al.  Extracellular superoxide dismutase (ecSOD) in vascular biology: an update on exogenous gene transfer and endogenous regulators of ecSOD. , 2008, Translational research : the journal of laboratory and clinical medicine.

[9]  S. Ballinger Mitochondrial dysfunction in cardiovascular disease. , 2005, Free radical biology & medicine.

[10]  T. Vanden Hoek,et al.  Significant levels of oxidants are generated by isolated cardiomyocytes during ischemia prior to reperfusion. , 1997, Journal of molecular and cellular cardiology.

[11]  R. Ross The pathogenesis of atherosclerosis: a perspective for the 1990s , 1993, Nature.