Kosugi K, Morel D W, DiCorleto P E, Chisolm G M
J Cell Physiol. 1987 Mar;130(3):311-20. doi: 10.1002/jcp.1041300302.
Oxidized LDL (o-LDL) is toxic to a variety of cultured cells. Preliminary results suggested that susceptibility is enhanced by cell proliferation. As a step toward determining the mechanism of cytotoxicity, we chose to identify the cell cycle phase(s) during which exposure of cultured human fibroblasts to o-LDL leads to death. Cytochalasin B, which blocks cell migration and proliferation, and irradiation, which prevents mitosis but not migration, both blocked cytotoxicity. Colchicine, which arrests cells in mitosis but does not inhibit DNA synthesis, did not block cytotoxicity. Treatment of cells with hydroxyurea, which blocks cells prior to S phase, prevented cell death. Addition of o-LDL to cells immediately after S phase allowed mitosis without death. The above results coupled with results using cells synchronized by three different means indicate that cell death is selective for proliferating cells and occurs after exposure to o-LDL during S phase. Understanding the mechanism of o-LDL-induced death may have implications for tissue damage in vivo in the numerous instances of pathology in which oxidized lipoproteins or lipids are present.
氧化型低密度脂蛋白(o-LDL)对多种培养细胞具有毒性。初步结果表明,细胞增殖会增强细胞对其的易感性。作为确定细胞毒性机制的第一步,我们选择确定培养的人成纤维细胞暴露于o-LDL导致死亡的细胞周期阶段。细胞松弛素B可阻断细胞迁移和增殖,而辐射可阻止有丝分裂但不影响迁移,二者均能阻断细胞毒性。秋水仙碱可使细胞停滞于有丝分裂期但不抑制DNA合成,它并不能阻断细胞毒性。用羟基脲处理细胞,可在S期之前阻断细胞,从而防止细胞死亡。在S期后立即向细胞中添加o-LDL可使细胞进行有丝分裂而不死亡。上述结果以及使用通过三种不同方法同步化的细胞所得到的结果表明,细胞死亡对增殖细胞具有选择性,并且发生在S期暴露于o-LDL之后。了解o-LDL诱导死亡的机制可能对体内存在氧化脂蛋白或脂质的众多病理情况下的组织损伤具有重要意义。