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目的探讨三氧化二砷诱导白血病及实体瘤细胞凋亡的机制。方法以三氧化二砷敏感和不敏感人食管癌细胞株为模型，运用ＲＴ－ＰＣＲ和流式细胞术检测三氧化二砷处理的这两类细胞Ｆａｓ／ＦａｓＬ表达的改变；同时利用荧光探针检测线粒体功能变化。结果两类细胞有同等水平Ｆａｓ表达，但均未检测出ＦａｓＬ；三氧化二砷既不能上调Ｆａｓ也不能诱导ＦａｓＬ表达，但破环线粒体跨膜电势和氧化－还原系统。结论三氧化二砷诱导人食管癌细胞凋亡不依赖Ｆａｓ／ＦａｓＬ的启动，而直接作用于线粒体，活化Ｃａｓｐａｓｅ－３导致凋亡。
Objective To investigate the mechanism of apoptosis induced by arsenic trioxide in leukemia and solid tumor cells. Methods The arsenic trioxide sensitive and insensitive human esophageal cancer cell lines were used as models. RT-PCR and flow cytometry were used to detect the changes of Fas/FasL expression in arsenic trioxide-treated cells. Fluorescence probes were used to detect mitochondrial function changes. Results Both types of cells had the same level of Fas expression, but no FasL was detected. Arsenic trioxide can neither up-regulate Fas nor FasL expression, but break the mitochondrial transmembrane potential and oxidation-reduction system. Conclusion The arsenic trioxide induced apoptosis of human esophageal carcinoma cells does not depend on the initiation of Fas/FasL, but directly acts on the mitochondria and activates Caspase-3 to induce apoptosis.