Effects of exposure to a time-varying 1.5 T magnetic field on the neurotransmitter-activated increase in intracellular Ca(2+) in relation to actin fiber and mitochondrial functions in bovine adrenal chromaffin cells.
BACKGROUND
It has been reported that exposure to electromagnetic fields influences intracellular signal transduction. We studied the effects of exposure to a time-varying 1.5 T magnetic field on membrane properties, membrane cation transport and intracellular Ca(2+) mobilization in relation to signals. We also studied the mechanism of the effect of exposure to the magnetic field on intracellular Ca(2+) release from Ca(2+) stores in adrenal chromaffin cells.


METHODS
We measured the physiological functions of ER, actin protein, and mitochondria with respect to a neurotransmitter-induced increase in Ca(2+) in chromaffin cells exposed to the time-varying 1.5 T magnetic field for 2h.


RESULTS
Exposure to the magnetic field significantly reduced the increase in [Ca(2+)]i. The exposure depolarized the mitochondria membrane and lowered oxygen uptake, but did not reduce the intracellular ATP content. Magnetic field-exposure caused a morphological change in intracellular F-actin. F-actin in exposed cells seemed to be less dense than in control cells, but the decrease was smaller than that in cytochalasin D-treated cells. The increase in G-actin (i.e., the decrease in F-actin) due to exposure was recovered by jasplakinolide, but inhibition of Ca(2+) release by the exposure was unaffected.


CONCLUSIONS
These results suggest that the magnetic field-exposure influenced both the ER and mitochondria, but the inhibition of Ca(2+) release from ER was not due to mitochondria inhibition. The effect of eddy currents induced in the culture medium may indirectly influence intracellular actin and suppress the transient increase in [Ca(2+)]i.
Ikehara
Toshitaka
T
Department of Human Welfare, Faculty of Health and Welfare, Tokushima Bunri University, Yamashiro-cho, Tokushima 770-8514, Japan. ikehara@tks.bunri-u.ac.jp
Nishisako
Hirotaka
H
Minami
Yuki
Y
Ichinose Sasaki
Hiromi
H
Shiraishi
Tairo
T
Kitamura
Mitsuo
M
Shono
Masayuki
M
Houchi
Hitoshi
H
Kawazoe
Kazuyoshi
K
Minakuchi
Kazuo
K
Yoshizaki
Kazuo
K
Kinouchi
Yohsuke
Y
Miyamoto
Hiroshi
H
D000109:Acetylcholine / Q000494:pharmacology*; D008841:Actin Cytoskeleton / Q000187:drug effects* / Q000378:metabolism; D000199:Actins / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000311:Adrenal Glands / Q000166:cytology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured; D019439:Chromaffin Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology; D015638:Cytochalasin D / Q000494:pharmacology; D047630:Depsipeptides / Q000494:pharmacology; D004574:Electromagnetic Fields; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D015151:Immunoblotting; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D018613:Microscopy, Confocal; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology; D018377:Neurotransmitter Agents / Q000494:pharmacology; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D013997:Time Factors; D050257:Tubulin Modulators / Q000494:pharmacology
D000199:Actins; D047630:Depsipeptides; D018377:Neurotransmitter Agents; D019384:Nucleic Acid Synthesis Inhibitors; D050257:Tubulin Modulators; C057531:jasplakinolide; D015638:Cytochalasin D; D000255:Adenosine Triphosphate; D000109:Acetylcholine; D003078:Colchicine; D002118:Calcium