title: Effects of a time-varying strong magnetic field on transient increase in Ca2+ release induced by cytosolic Ca2+ in cultured pheochromocytoma cells.
abstract: Exposure of pheochromocytoma (PC 12) cells to a time-varying 1.51 T magnetic field inhibited an increase in the intracellular Ca2+ concentration ([Ca2+]i) induced by addition of caffeine to Ca(2+)-free medium. This inhibition occurred after a 15-min exposure and was maintained for at least 2 h. [Ca2+]i sharply increased in cells loaded with cyclic ADP-ribose, and 2-h exposure significantly suppressed the increase. Addition of ATP induced a transient increase in intracellular Ca2+ release mediated by IP3 receptor, and this increase was strongly inhibited by the exposure. Results indicated that the magnetic field exposure strongly inhibited Ca2+ release mediated by both IP3 and ryanodine receptors in PC 12 cells. However, thapsigargin-induced Ca2+ influx (capacitative Ca2+ entry) across the cell membrane was unaffected. The ATP content was maintained at the normal level during the 2-h exposure, suggesting that ATP hydrolysis was unchanged. Therefore, Mg2+ which is known to be released by ATP hydrolysis and inhibit intracellular Ca2+ release may not relate the exposure-caused inhibition. Eddy currents induced in culture medium appear to change cell membrane properties and indirectly inhibit Ca2+ release from endoplasmic reticulum and other Ca2+ stores in PC 12 cells.
authors.affiliation: Department of Physiology, Pathophysiological Preventive Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
authors.forename: Toshitaka
authors.initials: T
authors.lastname: Ikehara
authors.forename: Hisao
authors.initials: H
authors.lastname: Yamaguchi
authors.forename: Keiko
authors.initials: K
authors.lastname: Hosokawa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Houchi
authors.forename: Ki Ho
authors.initials: KH
authors.lastname: Park
authors.forename: Kazuo
authors.initials: K
authors.lastname: Minakuchi
authors.forename: Hideki
authors.initials: H
authors.lastname: Kashimoto
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Kitamura
authors.forename: Yohsuke
authors.initials: Y
authors.lastname: Kinouchi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Yoshizaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Miyamoto
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D002413:Cations, Divalent / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D036563:Cyclic ADP-Ribose / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006868:Hydrolysis; D053496:Inositol 1,4,5-Trisphosphate Receptors; D019344:Lactic Acid / Q000096:biosynthesis; D008280:Magnetics; D016716:PC12 Cells; D051381:Rats; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D019284:Thapsigargin / Q000494:pharmacology; D013997:Time Factors
chemical_list: D015220:Calcium Channels; D002413:Cations, Divalent; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018160:Receptors, Cytoplasmic and Nuclear; D019837:Ryanodine Receptor Calcium Release Channel; D036563:Cyclic ADP-Ribose; D019344:Lactic Acid; D002110:Caffeine; D019284:Thapsigargin; D000255:Adenosine Triphosphate; D002118:Calcium