Тип публикации: статья из журнала

Год издания: 2008

Идентификатор DOI: 10.1007/s10517-008-0071-0

Ключевые слова: Apoptosis, Mitochondrion, Oxidative stress, Reactive oxygen forms, Receptor, annexin, reactive oxygen metabolite, transforming growth factor alpha receptor, aerobic metabolism, article, blood cell count, cell activation, cell membrane transport, cellular stress response, clinical article, community acquired pneumonia, controlled study, human, membrane potential, metabolic inhibition, mononuclear cell, protein expression, receptor binding, signal transduction, Humans, Leukocytes, Mononuclear, Membrane Potentials, Pneumonia, Reactive Oxygen Species, Receptors, Tumor Necrosis Factor, Type I

Аннотация: We studied mitochondrial and type 1 tumor necrosis factor-? 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 TNFR1-presentПоказать полностьюing cells and mononuclear cells with reduced mitochondrial transmembrane potential in case of induction of oxidative stress with 1 mM H2 O2 in vitro and in patients with pneumonia. © Springer Science+Business Media, Inc. 2008.

Журнал: Bulletin of Experimental Biology and Medicine

Выпуск журнала: Vol. 145, Is. 3

Номера страниц: 283-286

• Novitsky V.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Federal)
• Ryazantseva N.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Fede)
• Chasovskih N.Yu. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Fede)
• Starikova E.G. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Federa)
• Kaygorodova E.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Fede)
• Starikov Yu.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Federa)
• Jukova O.B. (Department of Pathophysiology, Siberian State Medical University, Federal Agency for Health Care and Social Development, Tomsk, Russian Federation, Department of Fundamentals of Clinical Medicine, Siberian State Medical University, Federal A)

• Scopus