Dexamethasone apoptosis induction and glucocorticoid receptor levels in cultured normal and neoplastic cell lines

The deletion with apoptotic mechanisms, of different normal and neoplastic cell lines [Jurkat leukemic cells, EUE epithelioid cells, normal (FG) and transformed rat fibroblasts (SGS/3A)] cultured in vitro in presence of dexamethasone, have been studied combining morphocytochemical (fluorescence microscopy), cytometric (flow cytometry) and biochemical (Radio Receptor Assay) analyses. It has been found that the synthetic glucocorticoid hormone induces an antiproliferative effect with accumulation of cells in the G1 phase and a cell loss by programmed death in some cell lines. The apoptotic incidence was found to be inversely proportional to the cytostatic effect of the hormone: the highest in EUE and Jurkat cells (in EUE cells not only affecting the G0/G1 phase of the cell cycle), the lowest in SGS/3A cells and absent in frbroblasts FG. The apoptotic degeneration, in all the cell lines studied, was characterized, morphologically and cytochemically by: a) decrease in stainability/content of cell DNA and proteins; b) condensation of cytoplasm; c) preservation of mitochondrial membrane functional integrity. In conclusion, in the presence of dexamethasone, programmed cell death was found to play a variable role during the maintenance of culture turnover in different cell lines and the incidence of degenerative phenomena does not appear to be related to glucocorticoid receptor levels.