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.