Chang M C, Ho Y S, Lee P H, Chan C P, Lee J J, Hahn L J, Wang Y J, Jeng J H
Team of Biomedical Science, Chang-Gung Institute of Nursing, Taiwan.
Carcinogenesis. 2001 Sep;22(9):1527-35. doi: 10.1093/carcin/22.9.1527.
There are 600 million betel quid (BQ) chewers in the world. BQ chewing is a major etiologic factor of oral cancer. Areca nut (AN) and arecoline may inhibit the growth of oral mucosal fibroblasts (OMF) and keratinocytes. In this study, AN extract (100-800 microg/ml) and arecoline (20-120 microM) inhibited the growth of oral KB cells by 36-90 and 15-75%, respectively. Exposure to arecoline (> 0.2 mM) for 24 h induced G(2)/M cell cycle arrest of OMF and KB cells. Areca nut extract (> 400 microg/ml) also induced G(2)/M arrest of KB cells, being preceded by S-phase arrest at 7-h of exposure. No evident sub-G(0)/G(1) peak was noted. Marked retraction and intracellular vacuoles formation of OMF and KB cells were observed. Glutathione (GSH) level, mitochondrial membrane potential (Deltabetam) and H(2)O(2) production of KB cells were measured by flow cytometry. GSH level [indicated by 5-chloromethyl-fluorescein (CMF) fluorescence] was depleted by 24-h exposure of KB cells to arecoline (0.4-1.2 mM) and AN extract (800-1200 microg/ml), with increasing the percentage of cells in low CMF fluorescence. By contrast, arecoline (0.1-1.2 mM) and AN extract (800-1200 microg/ml) induced decreasing and increasing H(2)O(2) production (by 2',7'-dichloro- fluorescein fluorescence), respectively. Hyperpolarization of Deltabetam (increasing of rhodamine uptake) was noted by 24-h exposure of KB cells to arecoline (0.4-1.2 mM) and AN extract (800-1200 microg/ml). AN extract (100- 1200 microg/ml) and arecoline (0.1-1.2 mM) induced little DNA fragmentation on KB cells within 24 h. These results indicate that AN ingredients are crucial in the pathogenesis of oral submucous fibrosis (OSF) and oral cancer by differentially inducing the dysregulation of cell cycle control, Deltabetam, GSH level and intracellular H(2)O(2) production, these events being not coupled with cellular apoptosis.
全球有6亿槟榔咀嚼者。咀嚼槟榔是口腔癌的主要病因。槟榔和槟榔碱可能会抑制口腔黏膜成纤维细胞(OMF)和角质形成细胞的生长。在本研究中,槟榔提取物(100 - 800微克/毫升)和槟榔碱(20 - 120微摩尔)分别使口腔KB细胞的生长抑制了36% - 90%和15% - 75%。槟榔碱(> 0.2毫摩尔)作用24小时可诱导OMF和KB细胞发生G(2)/M期细胞周期阻滞。槟榔提取物(> 400微克/毫升)也可诱导KB细胞发生G(2)/M期阻滞,且在暴露7小时时先出现S期阻滞。未观察到明显的亚G(0)/G(1)峰。观察到OMF和KB细胞出现明显的收缩和细胞内空泡形成。通过流式细胞术检测KB细胞的谷胱甘肽(GSH)水平、线粒体膜电位(ΔΨm)和H(2)O(2)产生量。KB细胞暴露于槟榔碱(0.4 - 1.2毫摩尔)和槟榔提取物(800 - 1200微克/毫升)24小时后,GSH水平(以5 - 氯甲基荧光素(CMF)荧光表示)降低,低CMF荧光的细胞百分比增加。相比之下,槟榔碱(0.1 - 1.2毫摩尔)和槟榔提取物(800 - 1200微克/毫升)分别诱导H(2)O(2)产生量降低和增加(以2',7' - 二氯荧光素荧光表示)。KB细胞暴露于槟榔碱(0.4 - 1.2毫摩尔)和槟榔提取物(800 - 1200微克/毫升)24小时后,观察到ΔΨm超极化(罗丹明摄取增加)。槟榔提取物(100 - 1200微克/毫升)和槟榔碱(0.1 - 1.2毫摩尔)在24小时内对KB细胞几乎未诱导DNA片段化。这些结果表明,槟榔成分通过差异性诱导细胞周期调控、ΔΨm、GSH水平和细胞内H(2)O(2)产生的失调,在口腔黏膜下纤维化(OSF)和口腔癌的发病机制中起关键作用,而这些事件与细胞凋亡无关。