Effects of a time-varying strong magnetic field on transient increase in Ca2+ release induced by cytosolic Ca2+ in cultured pheochromocytoma cells

• Published in: Biochimica et biophysica acta Vol. 1724; no. 1-2; pp. 8 - 16
• Main Authors: Ikehara, Toshitaka, Yamaguchi, Hisao, Hosokawa, Keiko, Houchi, Hitoshi, Park, Ki Ho, Minakuchi, Kazuo, Kashimoto, Hideki, Kitamura, Mitsuo, Kinouchi, Yohsuke, Yoshizaki, Kazuo, Miyamoto, Hiroshi
• Format: Journal Article
• Language: English
• Published: Netherlands 20.06.2005
• Subjects: Adenosine Triphosphate - metabolism; Adenosine Triphosphate - pharmacology; Animals; Caffeine - pharmacology; Calcium - metabolism; Calcium Channels - metabolism; Cations, Divalent - metabolism; Cell Membrane - metabolism; Cyclic ADP-Ribose - pharmacology; Cytosol - metabolism; Endoplasmic Reticulum - metabolism; Hydrolysis; Inositol 1,4,5-Trisphosphate Receptors; Lactic Acid - biosynthesis; Magnetics; PC12 Cells; Rats; Receptors, Cytoplasmic and Nuclear - metabolism; Ryanodine Receptor Calcium Release Channel - metabolism; Thapsigargin - pharmacology; Time Factors
• ISSN: 0304-4165; 0006-3002
• DOI: 10.1016/j.bbagen.2005.03.008

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.