Redox-dependent signal system in regulation of apoptosis under oxidative stress

The programmed cell death of peripheral blood mononuclear cells derived from donors with acute inflammatory diseases (acute appendicitis, community-acquired pneumonia) has been investigated in vitro under oxidative stress and selective inhibition of JNK MAP kinases and p38. Active and inactive MAP kinases and transcription factors p53 and NF-κB were assessed by immunoblotting. Apoptosis induced by oxidative stress in vitro and observed in acute inflammatory diseases is accompanied by increased level of reactive oxygen species (ROS) in cells. Inhibitors of JNK MAP kinase (SP600125) and p38 (ML3403) reduced the number annexin-positive mononuclear leucocytes under oxidative stress in vitro. This is evidence that JNK MAP-kinase and p38 are implicated in regulation mechanisms of oxidative apoptosis. Both p53 and NF-κB increased the number of apoptotic annexin-positive mononuclear leucocytes; however, NF-κB was revealed both in mononuclear leucocytes under oxidative stress in vitro and in cells isolated from donors with acute inflammatory, whereas p53 was only registered in cells under oxidative stress in vitro. It shows that NF-κB is not involved in antiapoptotic regulation. © Pleiades Publishing, Ltd. 2009.