title: [The role of redox-dependent signal systems in the regulation of apoptosis under oxidative stress condition].
abstract: 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. The action of inhibitors of MAP-kinases JNK (SP600125) and p38 (ML3403) in vitro under condition of oxidative stress prevents increase in the quantity of annexin-positive mononuclear leucocytes that testifies to involving JNK and p38 MAP-kinases in apoptosis deregulation oxidative mechanisms. The appearance of NF-kappaB in the mononuclear leucocytes under condition of oxidative stress during the acute inflammatory diseases and at the experiment was shown; p53 was registered only under condition of oxidative stress in vitro. The effect of p53 and NF-kappaB results in the increase in the quantity of apoptosis annexin-positive mononuclear leucocytes that testify to inoperativeness of antiapoptotic regulation NF-kappaB.
authors.forename: N V
authors.initials: NV
authors.lastname: Riazantseva
authors.forename: V V
authors.initials: VV
authors.lastname: Novitskiĭ
authors.forename: N Iu
authors.initials: NIu
authors.lastname: Chasovskikh
authors.forename: E V
authors.initials: EV
authors.lastname: Kaĭgorodova
authors.forename: E G
authors.initials: EG
authors.lastname: Starikova
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Starikov
authors.forename: T T
authors.initials: TT
authors.lastname: Radzivil
authors.forename: N V
authors.initials: NV
authors.lastname: Krat
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis; D001064:Appendicitis / Q000378:metabolism; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D048670:MAP Kinase Kinase 4 / Q000378:metabolism / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism / Q000502:physiology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011014:Pneumonia / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism / Q000502:physiology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism / Q000502:physiology*
chemical_list: D016328:NF-kappa B; D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D006861:Hydrogen Peroxide; D048051:p38 Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4