New silver(i) compounds containing 2-formylpyridine-N(4)-R-thiosemicarbazones and 1,10-phenanthroline (phen) were synthesized and characterized by spectroscopic techniques (IR and NMR), elemental analysis, ESI-MS and molar conductance measurements. In these complexes, both phen and thiosemicarbazone ligands are coordinated in a chelating bidentate fashion. Compounds 1-3 not only showed good in vitro antiproliferative activity against human lung (A549) and breast tumor cells (MDA-MB-231 and MCF-7), with IC50 values ranging from 1.49 to 20.90 μM, but were also demonstrated to be less toxic towards human breast non-tumor cells (MCF-10A). Cellular uptake studies indicated that compounds 1-3 were taken up by the MDA-MB-231 cells in 6 hours. Cell death assays in the MDA-MB-231 cells were conducted with compound 1 aiming to evaluate its effects on cell morphology, induction of apoptosis, the cell cycle, reactive oxygen species (ROS) formation and mitochondrial membrane potential (Δψm). Compound 1 caused morphological changes, such as cell shrinkage and rounding, increased the sub-G1 phase population, and induced apoptotic cell death, ROS formation and loss of mitochondrial membrane potential (Δψm). DNA binding results revealed that 1 interacted with the ct-DNA minor groove. Complexes 1-3 also exhibited good in vitro activity against M. tuberculosis H37Rv, with MIC values ranging from 3.37 to 4.65 μM.

中文翻译：

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带有2-甲酰基吡啶硫代半脲酮和1,10-菲咯啉的三元银（i）配合物的细胞毒性和凋亡作用。

合成了新的含2-甲酰基吡啶-N（4）-R-硫代半氨基甲酮和1,10-菲咯啉（phen）的银（i）化合物，并通过光谱技术（IR和NMR），元素分析，ESI-MS和摩尔电导进行了表征测量。在这些络合物中，phen和thiosemicarbazone配体均以螯合双齿的方式配位。化合物1-3不仅对人肺（A549）和乳腺肿瘤细胞（MDA-MB-231和MCF-7）表现出良好的体外抗增殖活性，IC50值在1.49至20.90μM之间，而且还被证明是对人乳腺非肿瘤细胞（MCF-10A）的毒性较小。细胞摄取研究表明，化合物1-3在6小时内被MDA-MB-231细胞摄取。使用化合物1在MDA-MB-231细胞中进行细胞死亡试验，旨在评估其对细胞形态，细胞凋亡诱导，细胞周期，活性氧（ROS）形成和线粒体膜电位（Δψm）的影响。化合物1引起形态变化，例如细胞缩小和​​变圆，增加了G1亚期的种群，并诱导了凋亡细胞的死亡，ROS的形成和线粒体膜电位（Δψm）的损失。DNA结合结果显示1与ct-DNA小沟相互作用。配合物1-3也表现出良好的针对结核分枝杆菌H37Rv的体外活性，MIC值为3.37至4.65μM。例如细胞收缩和舍入，增加了亚G1期细胞的数量，并诱导了凋亡细胞的死亡，ROS的形成和线粒体膜电位（Δψm）的损失。DNA结合结果显示1与ct-DNA小沟相互作用。配合物1-3也表现出良好的针对结核分枝杆菌H37Rv的体外活性，MIC值为3.37至4.65μM。例如细胞收缩和舍入，增加了亚G1期细胞的数量，并诱导了凋亡细胞的死亡，ROS的形成和线粒体膜电位（Δψm）的损失。DNA结合结果显示1与ct-DNA小沟相互作用。配合物1-3也表现出良好的针对结核分枝杆菌H37Rv的体外活性，MIC值为3.37至4.65μM。