The Role of Redox Status Changes in Dexamethasone-Induced Apoptosis in Jurkat Tumor Cells.

Abstract

The apoptotic death and its regulation was studied in intact Jurkat tumor cells and under the influence of buthionine-sulfoximine (de novo glutathione synthesis inhibitor; 1 mM) and/or apoptosis inducer dexamethasone (10 μM). The role of glutathione system components in dexamethasone-induced apoptosis in Jurkat tumor cells (both receptor-mediated and mitochondrial pathways) was analyzed. Under conditions of dexamethasone-induced apoptosis, glutathione system blockage mostly affects presentation of TNF RI- and Fas-receptors in Jurkat tumor cells, as well as change in content of transcription factors Apaf-1 and NF-κB, thereby promoting cell death. The decrease in the content of oxidized glutathione produced a potentiating effect on dexamethasone-induced apoptotic death of Jurkat tumor cells.