CYCLIC AMP-LEVELS OF RETINOIC ACID PRIMED HL-60 CELLS IN SERUM-FREE MEDIUM INFLUENCED BY A 50 HZ MAGNETIC-FIELD ALONE AND AS COFACTOR TO PROSTAGLANDIN E-2

In the present study, the human cell line HL-60 was induced to differe ntiation to mature granulocytes by the treatment with retinoic acid an d prostaglandin E-2 in physiological concentration. During the process of priming with retinoic acid and differentiation with prostaglandin E-2 changes in the concentration of the intracellular second messenger , cyclic adenosin monophosphate, plays a certain role among changes in the other signal transduction pathways. Analysis of the time sequence of cyclic adenosin monophosphate levels showed that in serum-free med ium the concentration temporarily increased, when HL-60 cells were inc ubated for 5 min with 10 nM retinoic acid. 24 h later the cells are on control level again. Priming with retinoic acid had no lasting influe nce on the rate of cell proliferation. When retinoic acid primed cells were incubated later for 5 min with 10 nM prostaglandin E-2, their cy clic adenosin monophosphate levels increased more pronounced. In the f ollowing 72-96 h, the cell proliferation was slowed down due to this t reatment with prostaglandin E-2. In comparison, a single exposure of r etinoic acid primed cells for 5 min to a 50 Hz magnetic field with 2 m T flux density led to a small, but statistical significant increase of the cyclic adenosin monophosphate level, similar to that observed aft er the treatment with retinoic acid, 24 h before. In combination with prostaglandin E-2, the magnetic field superimposed the cyclic adenosin monophosphate induced rise due to prostaglandin E-2, acting in an add itive way. Finally, when HL-60 cells were once treated with the 2 mT m agnetic field for 60 min, their growth rate was reduced without a loss of cell viability, but not until 144 h after the field treatment. Thi s was found in both absence and presence of prostaglandin E-2. In conc lusion, the magnetic field produced a small, but similar effect compar ed to that of prostaglandin E-2 and acted as an additive, when used as co-factor. (C) 1997 Elsevier Science S.A.