Chang Hong-Tai, Liu Chung-Shin, Chou Chiang-Ting, Hsieh Ching-Hong, Chang Chih-Hung, Chen Wei-Chuan, Liu Shiuh-Inn, Hsu Shu-Shong, Chen Jin-Shyr, Jiann Bang-Ping, Jan Chung-Ren
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.
Pharmacol Res. 2005 Oct;52(4):328-33. doi: 10.1016/j.phrs.2005.05.006.
The effect of the oxidizing agent thimerosal on cytosolic free Ca(2+) concentration ([Ca(2+)]i) and proliferation has not been explored in human osteoblast-like cells. This study examined whether thimerosal alters Ca(2+) levels and causes cell death in MG63 human osteosarcoma cells. [Ca(2+)]i and cell death were measured using the fluorescent dyes fura-2 and WST-1, respectively. Thimerosal at concentrations above 5 microM increased [Ca(2+)]i in a concentration-dependent manner. The Ca(2+) signal was reduced by 80% by removing extracellular Ca(2+). The thimerosal-induced Ca(2+) influx was sensitive to blockade of La(3+), and dithiothreitol (50 microM) but was insensitive to nickel and several L-type Ca(2+) channel blockers. After pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor), thimerosal failed to induce [Ca(2+)]i rises. Inhibition of phospholipase C with 2 microM U73122 did not change thimerosal-induced [Ca(2+)]i rises. At concentrations of 5, 10 and 20 microM thimerosal killed 33, 55 and 100% cells, respectively. The cytotoxic effect of 5 microM thimerosal was reversed by 54% by prechelating cytosolic Ca(2+) with BAPTA. Collectively, in MG63 cells, thimerosal induced a [Ca(2+)]i rise by causing Ca(2+) release from endoplasmic reticulum stores and Ca(2+) influx from extracellular space. Furthermore, thimerosal can cause Ca(2+)-related cytotoxicity in a concentration-dependent manner.
氧化汞对人成骨样细胞胞质游离钙离子浓度([Ca(2+)]i)及增殖的影响尚未见研究报道。本研究检测了氧化汞是否会改变MG63人骨肉瘤细胞中的钙离子水平并导致细胞死亡。分别使用荧光染料fura-2和WST-1检测[Ca(2+)]i和细胞死亡情况。浓度高于5微摩尔的氧化汞以浓度依赖方式增加[Ca(2+)]i。去除细胞外钙离子后,钙离子信号降低了80%。氧化汞诱导的钙离子内流对镧(La(3+))和二硫苏糖醇(50微摩尔)的阻断敏感,但对镍和几种L型钙离子通道阻滞剂不敏感。用1微摩尔毒胡萝卜素(一种内质网钙离子泵抑制剂)预处理后,氧化汞未能诱导[Ca(2+)]i升高。用2微摩尔U73122抑制磷脂酶C并未改变氧化汞诱导的[Ca(2+)]i升高。浓度为5、10和20微摩尔的氧化汞分别导致33%、55%和100%的细胞死亡。用BAPTA预螯合胞质钙离子可使5微摩尔氧化汞的细胞毒性作用逆转54%。总体而言,在MG63细胞中,氧化汞通过引起内质网钙库释放钙离子和细胞外钙离子内流诱导[Ca(2+)]i升高。此外,氧化汞可呈浓度依赖性地引起与钙离子相关的细胞毒性。