Ikehara Toshitaka, Yamaguchi Hisao, Hosokawa Keiko, Houchi Hitoshi, Park Ki Ho, Minakuchi Kazuo, Kashimoto Hideki, Kitamura Mitsuo, Kinouchi Yohsuke, Yoshizaki Kazuo, Miyamoto Hiroshi
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.
Biochim Biophys Acta. 2005 Jun 20;1724(1-2):8-16. doi: 10.1016/j.bbagen.2005.03.008. Epub 2005 Apr 2.
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.
将嗜铬细胞瘤(PC 12)细胞暴露于时变的1.51 T磁场中,可抑制在无钙培养基中添加咖啡因所诱导的细胞内Ca2+浓度([Ca2+]i)升高。这种抑制作用在暴露15分钟后出现,并持续至少2小时。在加载环ADP - 核糖的细胞中,[Ca2+]i急剧增加,而2小时的暴露显著抑制了这种增加。添加ATP可诱导由IP3受体介导的细胞内Ca2+释放短暂增加,而这种增加受到暴露的强烈抑制。结果表明,磁场暴露强烈抑制了PC 12细胞中由IP3和兰尼碱受体介导的Ca2+释放。然而,毒胡萝卜素诱导的跨细胞膜Ca2+内流(容量性Ca2+内流)未受影响。在2小时的暴露过程中,ATP含量维持在正常水平,表明ATP水解未发生变化。因此,已知由ATP水解释放并抑制细胞内Ca2+释放的Mg2+可能与暴露引起的抑制无关。培养基中感应产生的涡电流似乎改变了细胞膜特性,并间接抑制了PC 12细胞内质网和其他Ca2+储存库中的Ca2+释放。