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尼古丁诱导人神经胶质瘤和胶质母细胞瘤细胞系细胞死亡过程中的钙动员

Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines.

作者信息

Yamamura M, Amano Y, Sakagami H, Yamanaka Y, Nishimoto Y, Yoshida H, Yamaguchi M, Ohata H, Momose K, Takeda M

机构信息

Department of Biochemistry, School of Medicine, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.

出版信息

Anticancer Res. 1998 Jul-Aug;18(4A):2499-502.

PMID:9703899
Abstract

Nicotine dose-dependently induced cytotoxicity in human glioma (KG-1-C) and glioblastoma (GBS-1, T98G) cell lines, but could not induce internucleosomal DNA cleavage, in contrast to apoptosing human myelogenous leukemic cell lines. Human glioma/glioblastoma cell lines thus might have a chromatin structure resistant to endonuclease digestion. Nicotine induced a rapid increase in the intracellular calcium concentration. Confocal experiments with Fluo-3 fluorescence revealed that nicotine elevated the free Ca2+ concentration in both nuclear and cytoplasmic regions of the cells, and the elevation of Ca2+ in the nuclear region was more pronounced than that of the cytoplasmic region. The present study suggests that nuclear accumulation of Ca2+ is an important initial step for cell death induction by nicotine.

摘要

尼古丁剂量依赖性地诱导人胶质瘤(KG-1-C)和胶质母细胞瘤(GBS-1、T98G)细胞系产生细胞毒性,但与凋亡的人骨髓性白血病细胞系不同,它不能诱导核小体间DNA裂解。因此,人胶质瘤/胶质母细胞瘤细胞系可能具有抗核酸内切酶消化的染色质结构。尼古丁可迅速提高细胞内钙浓度。用Fluo-3荧光进行的共聚焦实验表明,尼古丁提高了细胞核和细胞质区域的游离Ca2+浓度,且细胞核区域Ca2+的升高比细胞质区域更明显。本研究表明,Ca2+的核内积累是尼古丁诱导细胞死亡的重要初始步骤。

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