NALM-1 cells (a cell line derived from human pre-B leukemia) were exposed to the opioid pentapeptide methionine-enkephalin (Met-enkephalin) and/or to thiorphan, an inhibitor of the enzyme that degrades the enkephalins (membrane endopeptidase EC 3.4.24.11, CALLA, the CD10 marker). Metabolic and proliferative activity was assessed after 6, 24 and 48 h in microplates using a colorimetric assay with vital dye MTT. CD10 expression was determined by means of semi-quantitative RT-PCR. Exposure to the Met-enkephalin at concentrations of 10(-8)-10(-6) M for 6 h reduced the MTT-activity, and after 24 and 48 h the suppression waned. Thiorphan (5 x 10(-6) M) abrogated the suppressive effect of the enkephalin, and after 6 h converted suppression into stimulation. Met-enkephalin (10(-6) M) increased and thiorphan (2.5 x 10(-6)-10(-6) M) decreased expression of CD10 at the RNA level. Suppression of the MTT uptake was attributed to the products of Met-enkephalin degradation caused by the enzymatic activity of CD10.