Seven Cu(II) complexes with 5-pyridin-2-yl-[1,3]dioxolo[4,5-g]isoquinoline derivatives as ligands: [Cu₂(L¹)₂Cl₄] (1), [Cu(L²)Cl₂] (2), [Cu(L¹)(NO₃)₂] (3), [Cu(L²)(NO₃)₂] (4), [Cu(L³)Cl₂] (5), [Cu(L³)Br₂] (6) and [Cu(L³)(NO₃)₂] (7){L¹=9-nitro-5-pyridin-2-yl-[1,3]dioxolo[4,5-g]isoquinoline, L²=4-nitro-5-pyridin-2-yl-[1,3]dioxolo[4,5-g]isoquinoline, L³=9-bromo-5-pyridin-2-yl-[1,3]dioxolo[4,5-g]isoquinoline}, were synthesized and characterized. Their in vitro anticancer activities against T-24, MGC-80-3, HeLa, Hep-G2, A549 and SK-OV-3 were evaluated. Compared with their corresponding ligands, most of these complexes exhibited enhanced anticancer activities in contrast to their corresponding ligands and copper salt. Among them, complexes 1 and 3 displayed selective cytotoxicity to HeLa cells comparing with normal liver cell HL-7702, with IC₅₀ values of 5.03 ± 1.20 μM and 10.05 ± 0.52 μM, respectively. Complexes 1 and 3 inhibited telomerase activity by interacting with c-myc promoter elements, and therefore exerted their antitumor activity. Furthermore, complexes 1 and 3 could trigger cell apoptosis via disruption of mitochondrial pathway through notably increased reactive oxygen species (ROS) levels, loss of mitochondrial membrane potential (Δψ_m), increase of the cytochrome c and apaf-1, decrease of bcl-2, and activation of caspases 3/9. Complexes 1 and 3 exhibited enhanced cytotoxicity, presenting synergetic effect after the ligands coordinated to copper(II) center.

七个以5-吡啶-2-基-[1,3] dioxolo [4,5- g ]异喹啉衍生物为配体的Cu（II）配合物：[Cu ₂（L ¹）₂ Cl ₄ ]（1），[Cu （L ²）Cl ₂ ]（2），[Cu（L ¹）（NO ₃）₂ ]（3），[Cu（L ²）（NO ₃）₂ ]（4），[Cu（L ³）Cl ₂ ]（5），[Cu（L ³）Br ₂]（6）和[Cu（L ³）（NO ₃）₂ ]（7）{ L ¹ = 9-硝基-5-吡啶-2--2-基-[1,3]二氧代[4,5- g ]异喹啉，L ² = 4-硝基-5-吡啶-2-基-[1,3]二氧杂环戊[4,5- g ]异喹啉，L ³ = 9-溴-5-吡啶-2-基-[1,3合成并表征了] dioxolo [4,5- g ]异喹啉}。他们的体外评估了对T-24，MGC-80-3，HeLa，Hep-G2，A549和SK-OV-3的抗癌活性。与它们相应的配体相比，与它们相应的配体和铜盐相比，大多数这些配合物表现出增强的抗癌活性。其中，复合物1和3与正常肝细胞HL-7702相比，对HeLa细胞表现出选择性的细胞毒性，IC ₅₀值分别为5.03±1.20μM和10.05±0.52μM。复合物1和3通过与c-myc启动子元件相互作用抑制端粒酶活性，因此发挥其抗肿瘤活性。此外，复合物1和3可以经由通过显着增加的活性氧线粒体途径的破坏触发细胞凋亡（ROS）水平，线粒体膜电位（Δψ的损失_米），细胞色素的增加Ç和APAF-1，BCL-2的减少，和胱天蛋白酶的活化3/9。配合物1和3表现出增强的细胞毒性，在配体配位至铜（II）中心后表现出协同作用。