ABSTRACT
Effect of dexamethasone upon NADPH oxidase activity of murine thymocytes and the role of reactive oxygen species (ROS) were investigated in dexamethasone-induced thymocyte apoptosis. Hormonal stimulation of NADPH oxidase has been demonstrated in cell-free system (homogenate of thymocytes). The depletion of hydrogen peroxide, produced due to NADPH oxidase activity, with catalase addition has been shown to inhibit dexamethasone-induced thymocyte apoptosis. The key role of NADPH oxidase and NADPH oxidase-dependent ROS production in the development of lymphocyte apoptosis was confirmed in experiments with two inhibitors of this enzyme. It has been evidenced that both inhibitors used (diphenylene iodonium and cromolyn) violently inhibited glucocorticoid-induced lymphocyte apoptosis. The possibility of the direct extragenomic action of glucocorticoids upon ROS production in the cells is discussed, as well as the role of this effect in glucocorticoid-induced lymphocyte apoptosis.
