Six novel organotin phosphonate complexes, [(Me3Sn)4(HL1)4]n1, [(Me3Sn)2(HL2)2]n2, [(Me3Sn)2L3(H2O)]n3, [(Ph3Sn)(HL1)]64, [(Ph3Sn)2L2]n5 and [(Ph3Sn)2L3]66, derived from phosphonic acid ligands [NaHL1 = 1-C10H7OPO2(OH)Na, H2L2 = 1-C10H7PO(OH)2, H2L3 = 2-C10H7PO(OH)2], have been synthesized and characterized by elemental analysis, FT-IR, NMR (1H, 13C, 31P and 119Sn) spectroscopy and X-ray crystallography. The structural analysis reveals that complexes 1 and 5 display 1D infinite zig-zag chain structures, and complex 2 shows 1D right-handed helical chain structure, while complex 3 displays 1D left-handed helical chain structure. Complexes 4 and 6 are 24-membered macrocyclic rings interconnected by P, O and Sn atoms. Additionally, the molecules of complexes 1 and 3 are further linked through intermolecular π···π and O-H···O interaction into supramolecular structures, respectively. Furthermore, we preliminarily estimated in vitro cytostatic activity of complexes 1-6 against the human cervix tumor cells (HeLa), human hepatocellular carcinoma cells (HepG-2) and human normal breast cells (HBL-100). Importantly, the anti-proliferative properties and possible pathway of complex 6 are investigated, and the results demonstrate that complex 6 could induce apoptotic cell death via an overload of intracellular reactive oxygen species (ROS) levels and the dysfunctional depolarization of mitochondrial membranes.

中文翻译：

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基于膦酸配体的新型三有机锡复合物：合成，结构和体外细胞抑制活性。

六个新颖的有机锡膦酸酯络合物，[（Me3Sn）4（HL1）4] n1，[（Me3Sn）2（HL2）2] n2，[（Me3Sn）2L3（H2O）] n3，[（Ph3Sn）（HL1）] 64 ，[（Ph3Sn）2L2] n5和[（Ph3Sn）2L3] 66，衍生自膦酸配体[NaHL1 = 1-C10H7OPO2（OH）Na，H2L2 = 1-C10H7PO（OH）2，H2L3 = 2-C10H7PO（OH） ）2]，已通过元素分析，FT-IR，NMR（1H，13C，31P和119Sn）光谱和X射线晶体学合成并表征。结构分析表明，复合物1和5显示1D无限之字形链结构，复合物2显示1D右手螺旋链结构，而复合物3显示1D左手螺旋链结构。配合物4和6是由P，O和Sn原子互连的24元大环。另外，配合物1和3的分子通过分子间π··π和OH··O相互作用进一步连接成超分子结构。此外，我们初步估计了复合物1-6对人宫颈癌细胞（HeLa），人肝细胞癌细胞（HepG-2）和人正常乳腺细胞（HBL-100）的体外细胞抑制活性。重要的是，研究了复合物6的抗增殖特性和可能的​​途径，结果表明，复合物6可通过细胞内活性氧（ROS）水平超负荷和线粒体膜去极化功能异常诱导凋亡细胞死亡。人肝癌细胞（HepG-2）和人正常乳腺细胞（HBL-100）。重要的是，研究了复合物6的抗增殖特性和可能的​​途径，结果表明，复合物6可通过细胞内活性氧（ROS）水平超负荷和线粒体膜去极化功能异常诱导凋亡细胞死亡。人肝癌细胞（HepG-2）和人正常乳腺细胞（HBL-100）。重要的是，研究了复合物6的抗增殖特性和可能的​​途径，结果表明，复合物6可通过细胞内活性氧（ROS）水平超负荷和线粒体膜去极化功能异常诱导凋亡细胞死亡。