Banerjee P, Majumder P, Halder S, Drew M G B, Bhattacharya S, Mazumder S
Department of Biochemistry, University of Calcutta , India.
Free Radic Res. 2015 Mar;49(3):253-68. doi: 10.3109/10715762.2014.998665. Epub 2015 Jan 28.
In this study, we report the synthesis of four 2-(arylazo)phenol-Pd(II) complexes and their anti-proliferative property against the human lung cancer (A549), cervical cancer (HeLa), and ovarian teratocarcinoma (PA-1) cell lines with cisplatin as the gold standard. One of the complexes, [Pd(L(2))2], induced robust apoptosis in all the chosen cells, as revealed by annexin-V-positive/propidium iodide dual staining, increased sub-G1 cell cycle population, and significant morphological changes in the treated cells. The Pd complex inflicted mitochondrial dysfunction leading to mitochondrial membrane potential loss, reactive oxygen species generation and release of cytosolic cytochrome c that activated caspase-9 and caspase-3 proteins which finally caused programmed cell death.
在本研究中，我们报告了四种2-(芳基偶氮)苯酚-Pd(II)配合物的合成及其以顺铂为金标准对人肺癌(A549)、宫颈癌(HeLa)和卵巢畸胎癌(PA-1)细胞系的抗增殖特性。其中一种配合物[Pd(L(2))2]在所有选定的细胞中诱导了强烈的凋亡，这通过膜联蛋白V阳性/碘化丙啶双重染色、亚G1期细胞周期群体增加以及处理后细胞明显的形态变化得以揭示。该钯配合物导致线粒体功能障碍，导致线粒体膜电位丧失、活性氧生成以及胞质细胞色素c的释放，从而激活了caspase-9和caspase-3蛋白，最终导致程序性细胞死亡。
