Effect of low frequency electromagnetic fields on A2A and A3 adenosine receptors in human neutrophils.

The present study was designed to evaluate the binding and functional characterization of A2A and A3 adenosine receptors in human neutrophils exposed to low frequency, low energy, pulsing electromagnetic fields (PEMFs). Saturation binding experiments on A2A and A3 adenosine receptors revealed a single class of binding sites with similar affinity in control and in PEMF-treated human neutrophils (KD=1.050.10 and 1.080.12 nM for A2A receptors and KD=2.360.16 and 2.450.15 nM for A3 receptors, respectively). PEMFs treatment revealed that the A2A and A3 receptor density was statistically increased (Bmax=12610 and 21515* fmol mg-1 protein and Bmax=45118 and 73625* fmol mg-1 protein, respectively, *, P<0.01). In the adenylyl cyclase assays the A2A agonists, HE-NECA and NECA increased cAMP accumulation in untreated human neutrophils with an EC50 value of 43 (40-47) and 255 (228-284) nM, respectively. The capability of the examined compounds to stimulate cAMP levels in human neutrophils was increased after PEMF exposure with an EC50 value of 10 (8-13)* and 61 (52-71)* nM, respectively, *, P<0.01. In the superoxide anion production assays examined agonists inhibited the generation of O2- in untreated human neutrophils with an EC50 value of 3.6 (3.1-4.2) and of 23 (20-27) nM, respectively. In PEMF-treated human neutrophils, the same compounds show an EC50 value of 1.6 (1.2-2.1)* and of 6.0 (4.7-7.5)* nM, respectively, *, P