[Intracellular gaseous messengers, nitric oxide, carbon monoxide and hydrogen sulfide participate in apoptosis regulation].

In this paper, participation of gases, nitric oxide, carbon monoxide and hydrogen sulfide, in cell apoptosis regulation has been analyzed according to the literature data and our own findings. Different mechanisms of nitric oxide influence on apoptotic reaction including modulation of transcription factors activity and increase in mitochondrion membrane permeabilisation are described. Brief description of the generation and signal transduction pathways of carbon monoxide is presented.

[The role of nitric oxide synthesis induction and inhibition in regulation of blood neutrophil cell death during oxidative disbalance].

Modeling oxidative stress in vitro with 5mM H2O2 has demonstrated a protective role of nitric oxide on realization of constitutional blood neutrophil cell death. The NO-synthase inductor L-arginine and the inhibitor of nitric oxide synthesis, L-NAME, influenced on the amount of annexin-positive cells, the content of Bax protein, reactive oxygen species, cyclic nucleotides, and calcium homeostasis in neutrophils under conditions realizing programmed death during oxidative stress in vitro and under acute inflammation. During oxidative stress L-arginine normalized the increased intracellular Ca2+ level and the cAMP/cGMP ratio due to increase of cGMP level, stabilized metabolism and prolonged neutrophil life.

[The role of p53 and NF-kappaB transcription factors in redox-dependent dysregulation of mononuclear leukocyte apoptosis].

The aim of this work was to study programmed death of blood mononuclear leukocytes taken from healthy donors and patients with acute inflammatory diseases (acute appendicitis, community-acquired pneumonia). Cellular p53 and NF-kappaB transcription factors were detected by western blotting. Active form of NF-kappaB was shown to appear in mononuclear leukocytes undergoing oxidative stress in experiment and during acute inflammation, p53 was found only under oxidative stress conditions in vitro.

[The role of redox-dependent signal systems in the regulation of apoptosis under oxidative stress condition].

Programmed death of peripheral blood mononuclear cells from donors with acute inflammatory diseases (an acute appendicitis, a community-acquired pneumonia) was investigated under condition of oxidative stress in vitro and under effect of selective inhibitors of MAP-kinases JNK and p38. Levels of active and inactive forms of MAP-kinases, and factors of transcription were determined by immunoblotting (western blot analysis). The increase in the activity of apoptosis under condition of oxidative stress in vivo and during the acute inflammatory diseases is associated with the increase in the level of reactive oxygen species (ROS) in the cells.

[Redox-dependent regulation of apoptosis as a function of intracellular reactive oxygen species in oxidative stress].

Programmed cell death of mononuclear cells in conditions of oxidative stress in vitro and selective inhibitors of MAP-kinases JNK, p38 were investigated. Levels of active and inactive forms of MAP-kinases, factors of transcription P53, NF-kB and proteins-regulators of apoptosis Bcl-X(L), Bad, Bcl-2 were determined by immunoblotting (Western blotting). The increasing of number of annexin-plus mononuclears/lymphocytes in the culture associated with enhance of the level of intracellular reactive oxygen species was shown.

[Extrahospital pneumonias: the clinico-scintigraphic characterization and oxidative balance of cells].

Ventilation-perfusion pulmonary scintigraphy was carried out in 30 patients with a verified diagnosis of extra-hospital pneumonia (EHP) and 10 healthy subjects; ventilation-perfusion ratio (V/Q), apex-basis ventilation and perfusion gradient, and the condition of alveolar-capillary permeability (ACP) were analyzed. Clinical symptoms during the debut of EHP were more pronounced in patients with an alveolar type of pulmonary infiltrate (PI) vs. patients with interstitial one: they had pulmonary infiltration syndrome, pleural pain, tachypnoe, tachycardia, a fever of higher than 38 degrees C, and leucocytosis more often.

[Impaired oxidative metabolism in acute inflammatory diseases].

The specific features of lipid peroxidation (LPO) and the activity of enzymatic antioxidants in the plasma and red blood cells of patients with acute appendicitis, phlegmons, and abscesses located in the soft tissues of the shin, hip, buttocks, shoulder, and forearm were comprehensively evaluated. In these diseases, the signs of evolving oxidative stress were revealed irrespective of the site of an acute inflammatory focus. Excess accumulation of LPO products was recorded with the inhibition of antioxidative defense components, including erythrocytic glutathione-dependent enzymes.