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Pulsed electromagnetic fields affect the intracellular calcium concentrations in human astrocytoma cells
Author(s) -
Pessina G.P.,
Aldinucci C.,
Palmi M.,
Sgaragli G.,
Benocci A.,
Meini A,
Pessina F.
Publication year - 2001
Publication title -
bioelectromagnetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.435
H-Index - 81
eISSN - 1521-186X
pISSN - 0197-8462
DOI - 10.1002/bem.79
Subject(s) - caffeine , calcium , intracellular , bioelectromagnetics , chemistry , calcium in biology , biophysics , endocrinology , electromagnetic field , medicine , biochemistry , biology , physics , quantum mechanics , organic chemistry
Abstract Experiments assessed whether long term exposure to 50 Hz pulsed electromagnetic fields with a peak magnetic field of 3 mT can alter the dynamics of intracellular calcium in human astrocytoma U‐373 MG cells. Pretreatment of cells with 1.2 μM substance P significantly increased the [Ca 2+ ] i . The same effect was also observed when [Ca 2+ ] i was evaluated in the presence of 20 mM caffeine. After exposure to electromagnetic fields the basal [Ca 2+ ] i levels increased significantly from 143 ± 46 nM to 278 ± 125 nM. The increase was also evident after caffeine addition, but in cells treated with substance P and substance P + caffeine we observed a [Ca 2+ ] i decrease after exposure. When we substituted calcium‐free medium for normal medium immediately before the [Ca 2+ ] i measurements, the [Ca 2+ ] i was similar to that measured in the presence of Ca 2+ . In this case, after EMFs exposure of cells treated with substance P, the [Ca 2+ ] i , measured without and with addition of caffeine, declined from 824 ± 425 to 38 ± 13 nM and from 1369 ± 700 to 11 ± 4 nM, respectively, indicating that electromagnetic fields act either on intracellular Ca 2+ stores or on the plasma membrane. Moreover the electromagnetic fields that affected [Ca 2+ ] i did not cause cell proliferation or cell death and the proliferation indexes remained unchanged after exposure. Bioelectromagnetics 22:503–510, 2001. © 2001 Wiley‐Liss, Inc.