LACK OF PROTECTIVE EFFECT OF R(-)-DEPRENYL ON PROGRAMMED CELL-DEATH OF MOUSE THYMOCYTES INDUCED BY DEXAMETHASONE

R(-)-Deprenyl, an archetypical MAO-B inhibitor, has been shown to dela y the onset of the disabling syndrome of Parkinson's disease and to be useful in the treatment of Alzheimer's disease. Recently, R(-)-depren yl has been claimed to be capable of preventing apoptosis of PC12 cell s, which had been primed with nerve growth factor (NGF) and followed b y withdrawal of serum. We investigated the effect of R(-)-deprenyl in a non-neuronal fell model, namely, apoptosis of mouse thymocytes induc ed by dexamethasone. Trypan blue exclusion and lactate dehydrogenase a ctivity were applied to assess the cell survival. R(-)-Deprenyl did no t exhibit any detectable protective effect to the thymocytes from apop tosis. This result is further confirmed by examining the apoptotic DNA fragmentation using gel electrophoresis and assessing the soluble DNA released by a spectrophotometric method.