目的　研究抗癌抗生素力达霉素 (LDM )诱导人肝癌BEL 740 2细胞死亡的特征。方法　用荧光染料Hoechst 33342和PI联染 ;琼脂糖凝胶电泳检测 ;流式细胞术检测等。结果　LDM 1μmol·L-1处理该细胞后 6h ,可观察到一种有别于典型凋亡的染色质凝集方式 :核膜一直保持完整 ,细胞仍贴壁 ,无凋亡小体形成 ;琼脂糖凝胶电泳检测到DNA梯带。流式细胞术检测到的G1亚峰 ,仅在LDM处理BEL 740 2细胞后 2 4h出现。LDM处理BEL 740 2细胞后 6h ,caspase 3,6的活性分别增高 5 ,4倍。染色质开始凝集的时间比caspase 6活性达到高峰的时间早。结论　力达霉素诱导人肝癌BEL 740 2细胞死亡的特征有别于典型的凋亡 ,此结果可能有助于解释其极高活性地杀死肿瘤细胞的分子机制 Objective To study the characteristics of the death of human liver cancer BEL 740 2 cells induced by antitumor antibiotics, lidamycin (LDM). Methods Fluorescence dye Hoechst 33342 and PI were used for dyeing; agarose gel electrophoresis; flow cytometry and so on. Results After treated with LDM 1μmol·L-1 for 6 h, a kind of chromatin agglutination which was different from typical apoptosis could be observed: the nuclear membrane remained intact, the cells remained adherent, no apoptotic bodies were formed; agarose DNA ladders were detected by gel electrophoresis. The G1 sub-peak detected by flow cytometry appeared only 24 h after LDM treatment of BEL 740 2 cells. After LDM treatment of BEL 740 2 cells for 6 h, the activity of caspase 3,6 increased by 5 and 4 times, respectively. Chromatin begins to agglutinate earlier than the time when caspase 6 activity peaks. Conclusion The characteristics of human liver cancer BEL 740 2 cell death induced by lidamacin are different from the typical apoptosis. This result may help explain the molecular mechanism of its extremely active killing of tumor cells.