Effects on Rb(+)(K+) uptake of HeLa cells in a high K(+) medium of exposure to a switched 1.7 Tesla magnetic field.
Effects of a switched, time-varying 1.7 T magnetic field on Rb(+)(K+) uptake by HeLa S3 cells incubated in an isosmotic high K(+) medium were examined. The magnetic flux density was varied intermittently from 0.07-1.7 T at an interval of 3 s. K(+) uptake was activated by replacement of normal medium by high K(+) medium. A membrane-permeable Ca(2+) chelating agent (BAPTA-AM) and Ca(2+)-dependent K(+) channel inhibitors (quinine, charibdotoxin, and iberiotoxin) were found to reduce the Rb(+)(K+) uptake by about 30-40%. Uptake of K(+) that is sensitive to these drugs is possibly mediated by Ca(2+)-dependent K(+) channels. The intermittent magnetic field partly suppress ed the drug-sensitive K(+) uptake by about 30-40% (P < 0.05). To test the mechanism of inhibition by the magnetic fields, intracellular Ca(2+) concentration ([Ca(2+)]c) was measured using Fura 2-AM. When cells were placed in the high K(&plus;) medium, [Ca(2+)]c increased to about 1.4 times the original level, but exposure to the magnetic fields completely suppressed the increase (P < 0.01). Addition of a Ca(2+) ionophore (ionomycin) to the high K(+) medium increased [Ca(2+)]c to the level of control cells, regardless of exposure to the magnetic field. But the inhibition of K(+) uptake by the magnetic fields was not restored by addition of ionomycin. Based on our previous results on magnetic field-induced changes in properties of the cell membrane, these results indicate that exposure to the magnetic fields partly suppresses K(+) influx, which may be mediated by Ca(2+)-dependent K(+) channels. The suppress ion of K(+) fluxes could relate to a change in electric properties of cell surface and an inhibition of Ca(2+) influx mediated by Ca(2+) channels of either the cell plasma membrane or the inner vesicular membrane of intracellular Ca(2+) stores.
Ikehara
T
T
Department of Physiology, School of Medicine, The University of Tokushima, Tokushima, Japan.
Park
K H
KH
Yamaguchi
H
H
Hosokawa
K
K
Yoshizaki
K
K
Miyamoto
H
H
Aizawa
K
K
Kinouchi
Y
Y
D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000528:radiation effects; D002462:Cell Membrane / Q000187:drug effects / Q000528:radiation effects; D018999:Charybdotoxin / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D003470:Culture Media; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004574:Electromagnetic Fields; D004594:Electrophysiology; D004781:Environmental Exposure; D005456:Fluorescent Dyes; D016257:Fura-2; D006367:HeLa Cells; D006801:Humans; D007425:Intracellular Membranes / Q000187:drug effects / Q000528:radiation effects; D015759:Ionomycin / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008280:Magnetics; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000528:radiation effects; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000528:radiation effects; D011803:Quinine / Q000494:pharmacology; D012413:Rubidium / Q000378:metabolism* / Q000528:radiation effects
D002614:Chelating Agents; D003470:Culture Media; D005456:Fluorescent Dyes; D007476:Ionophores; D010455:Peptides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D018999:Charybdotoxin; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; D015759:Ionomycin; C064719:iberiotoxin; D011803:Quinine; D012413:Rubidium; D011188:Potassium; D002118:Calcium; D016257:Fura-2