Succinate and succinate dehydrogenase of mononuclear blood leukocytes as markers of adaptation of mitochondria to hypoxia in patients with exacerbation of chronic obstructive pulmonary disease

Aim . To study the concentration of succinate and the activity of succinate dehydrogenase (SDH) of mononuclear blood leukocytes as markers of rapid adaptation of mitochondria to hypoxia in patients with exacerbation of chronic obstructive pulmonary disease (COPD). Materials and Methods . The study involved 58 patients with COPD and 13 conventionally healthy volunteers of 40-75 years of age. In accordance with GOLD 2018 principles of complex assessment, the patients were divided to groups B (n=18), C (n=20), D (n=20) comparable in age, FEV 1 and in pack-of-cigarettes/year index. Patients of D group were characterized by more pronounced hypoxemia. Activity of SDH and concentration of succinate were determined in mononuclear leukocytes isolated from blood. Results. Patients with exacerbation of COPD divided to groups on the basis of the frequency of exacerbations and evidence of symptoms, were characterized by different severity of disorders of mitochondrial functions of mononuclear leukocytes. Patients of C group had the highest succinate concentration (428 [357;545] nmol/10 6 cells in I ml of suspension) and SDH activity (64[56;73] nmol of succinate/min * 10 6 cells of 1 ml of suspension) in mononuclear leukocytes as compared to groups B (1.43-times reduction of succinate, p<0.002; 1.88-times reduction of SDH, p=0.0015) and D (2.06-times reduction of succinate, p<0.0001; 4.26-times reduction of SDH, p<0.0001). Patients of D group demonstrated the most pronounced reduction of markers of adaptation to hypoxia. Conclusions. A small amount of symptoms in exacerbation of COPD is associated with the highest parameters of the mechanism of rapid adaptation of mitochondria of mononuclear leukocytes to hypoxia. Existence of evident symptoms and frequent exacerbations in patents is associated with a severe frustration of mechanisms of adaptation of mitochondria to hypoxia.