[VVO2(O2C14H6O2)(C5N2H12)](C5N2H13)(CH3OH) (1) and Na[VVO(O2C14H6O2)2][(CH3)2NCHO]}n (2) have been synthesized by the reaction of V2O5 and NaVO3 with aromatic 1,2-diol (1,2-dihydroxyanthraquinone), and their molecular and crystal structures have been determined by X-ray diffraction. MTT assay tests of the VVO2LALB and VVOL2 complexes against cancer cells have revealed that, when L is catechol, VOL2 showed broad-spectrum, high anticancer activities which were proportional to their concentration; however when L is naphthol or alizarin, VOL2 displayed little effect towards the cancer cells; moreover, complex 1 in the coordination model of VVO2LALB showed specifically higher inhibition (88.65%) against HCT-8 than the clinical anticancer drug Fu-5 (69.97%). The results revealed that both the V(V) and the ligands cannot influence the inhibition against cancer cells individually. The mechanism of the broad-spectrum anticancer activities of VOL2 when L is catechol ligand might originate from the redox activities of VV/VIV which regulate the concentration of ROS (reactive oxygen species). N-Methylpiperazine formed as a by-product in complex 1 was confirmed by 1H NMR and its formation mechanism catalyzed by V2O5 has been deduced.
[VVO2(O2C14H6O2)(C5N2H12)](C5N2H13)( OH) (1) 和 Na[VVO(O2C14H6O2)2][(
CH3)2NCHO]}n (2) 是通过 V2O5 和 NaVO3 与芳香族 1,2
-二醇(
1,2-二羟基蒽醌)的反应合成的,并通过 X 射线衍射确定了它们的分子和晶体结构。对 VVO2
LALB 和 VVO
L2 复合物进行的 M
TT 法检测显示,当
配体 L 为
儿茶酚时,VO
L2 显示出广谱、高抗癌活性,并与其浓度成正比;然而,当 L 为
萘醇或
茜素时,VO
L2 对癌细胞的效果较小。此外,复合物 1 在 VVO2
LALB 的配位模型中对 HCT-8 的抑制率(88.65%)明显高于临床抗癌药物 Fu-5(69.97%)。结果表明 V(V) 和
配体单独对癌细胞的抑制作用没有影响。当 L 为
儿茶酚配体时,VO
L2 的广谱抗癌活性机制可能源于 VV/VIV 的氧化还原活性,这些活性调节了 ROS(反应性氧种)的浓度。复合物 1 中形成的
N-甲基哌嗪作为副产物已通过 1H NMR 确认,并推导了由 V2O5 催化的形成机制。