Effect of polyamines on superoxide dismutase activity under dexamethasone-induced apoptosis in rat thymocytes.

The intracellular redox state is of importance for cell growth, differentiation, and apoptosis through reactive oxygen species (ROS) functioning as metabolic fine-tuner. Optimal levels of polyamines are necessary for growth, differentiation, and apoptotic cell death while they also protect cell from ROS accumulation. We have carried out studies to find out the interrelation between these two distant metabolic pathways. For that purpose, the glucocorticoid-triggered programmed cell death of rat thymocytes has been used. Our data confirm that SOD activity (which testifies both to the level of ROS generation and antioxidative defense state) changes in response to programmed cell death conditions and to alteration of intracellular polyamines level. Thymocytes death induced by dexamethasone is partially mediated by polyamines content. Our data prove that one of the molecular mechanisms of thymocytes population resistance after dexamethasone treatment is an enhanced level of antioxidant defense. It is evident that in dexamethasone-treated rat thymocytes polyamines modulate signal transduction processes to apoptosis development via changes in cellular redox status.