Apoptosis of blood neutrophils from healthy donors was studied under conditions of cell culturing with different concentrations of H(2)O(2), selective NO synthase inhibitor, and inductor of NO synthesis (L-arginine). In vitro incubation of neutrophilic leukocytes with 5 mM H(2)O(2) led to activation of the apoptotic program in neutrophils, which was seen from increased content of Bax protein in the cells and increased number of apoptotic cells in the culture. Increased content of annexin-positive cells after incubation of neutrophil culture with NO synthase inhibitor suggests involvement of NO in the regulation of neutrophil apoptosis under conditions of oxidative stress, while L-arginine prevented H(2)O(2)-induced programmed cell death.

Programmed death of peripheral blood mononuclear cells from healthy donors was studied during culturing with various concentrations of H(2)O(2) and selective inhibitors of JNK (SP600125) and p38 MAPK (ML3403). In vitro incubation of mononuclear leukocytes with 1 mM H(2)O(2) stimulated apoptotic cell death. Treatment with inhibitors (SP600125 and ML3403) during in vitro oxidative stress prevented the increase in the number of annexin-positive mononuclear cells. Our results indicate that MAP kinases JNK and p38 are involved in the mechanisms of oxidative dysregulation of apoptosis.

An ovigerous female of red king crab (Paralithodes camtschaticus) was caught near the White Sea

No abstract

We studied mitochondrial and type 1 tumor necrosis factor-a receptor (TNFR1)-mediated pathways triggering the apoptotic program in mononuclear cells under conditions of oxidative stress. Intensification of intracellular production of reactive oxygen forms is accompanied by an increase in the number of annexin-positive TNFRI-presenting cells and mononuclear cells with reduced mitochondrial transmembrane potential in case of induction of oxidative stress with 1 mM H2O2 in vitro and in patients with pneumonia.

No abstract

Investigation of influence of gases nitric oxide and hydrogen sulfide on apoptotic cell death of Jurlat cells and mononuclear leucocytes of healthy donors was conducted. It was shown that 100 mmol sodium nitroprussidi increased the apoptosis of T lymphoblast leukemia cells after 15’ incubation. 10 and 100 mmol donor of hydrogen sulfide caused apoptotic death of Jurkat cells after 15’ incubation. 15’ exposure of nitric oxide and hydrogen sulfide donors did not lead to the changes of cell death of mononuclear leucocytes. Gaseous transmitters NO and H2S increased necrosis of Jurkat cells and mononuclear leucocytes after 24 h incubation with the appropriate gase’s donor.

The aim of this study was to identify the features of CD4+ lymphocytes apoptosis in children with cryptosporidiosis. Feces for the detection of cryptosporidium and venous blood for the study of lymphocytes apoptosis were the material of the study. Mononuclear leukocytes were isolated from venous whole blood and cultured in a complete culture medium. Cells were incubated for 24 hours with inducers of the receptor (TNFα) and mitochondrial pathways of apoptosis (dexamethasone).Cryptosporidia have been found in 35% of acute intestinal infections in children. The number of lymphocytes with cytoflurimetric signs of apoptosis in the group of cryptosporidiosis-positive patients did not differ from that in patients without cryptosporidiosis (p=0.421). There were no intergroup differences in the number of CD4+ lymphocytes expressing the Fas receptor on their surface (p=0.462). In cultures incubated in the presence of dexamethasone, a decrease in the number of apoptotically altered CD4+ lymphocytes was registered only in the group of cryptosporidiosispositive patients (p=0.028).The study showed that in cryptosporidiosis, the sensitivity of CD4+ cells to the induction of the mitochondrial pathway of apoptosis changes in favor of slowing down this variant of cell death.