基于吡哆醛的钒(IV)配合物的治疗潜力，其对癌细胞具有选择性细胞毒性，而对健康细胞则没有。

Therapeutic potential of a pyridoxal-based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells.

机构信息

Department of Chemistry and Biology, University of Salerno, via Ponte Don Melillo, Fisciano SA, Italy.

出版信息

J Cell Physiol. 2013 Nov;228(11):2202-9. doi: 10.1002/jcp.24385.

Abstract

Vanadium compounds can exert anticancer effects, partly due to inhibition of tyrosine phosphatases. Here, we report the effect of N,N'-ethylenebis (pyridoxylideneiminato) vanadium (IV) complex (Pyr2 enV(IV)), that induced 93% and 57% of cell mortality in A375 (human melanoma) and A549 (human lung carcinoma) cells, respectively; the mortality was <24% in other cancer cell lines and in human normal epidermal keratinocytes, lung cells and peripheral blood mononuclear cells. The mechanism of Pyr2 enV(IV) effect relied on apoptosis induction; this was triggered by ROS increase, followed by mitochondrial membrane depolarization. Indeed, the addition of N-acetyl cysteine to cell cultures abated Pyr2 enV(IV)-induced apoptosis. These results disclose the pro-apoptotic activity of Pyr2 enV(IV) and its mechanism, relying on intracellular ROS increase.

摘要

钒化合物可以发挥抗癌作用，部分原因是抑制酪氨酸磷酸酶。在这里，我们报告了 N,N'-亚乙基双（吡啶醛亚氨基）钒（IV）配合物（Pyr2 enV(IV)）的作用，它分别诱导 A375（人黑色素瘤）和 A549（人肺癌）细胞 93%和 57%的细胞死亡率；在其他癌细胞系和人正常表皮角质形成细胞、肺细胞和外周血单核细胞中，死亡率<24%。 Pyr2 enV(IV)作用的机制依赖于细胞凋亡的诱导；这是由 ROS 增加引发的，随后是线粒体膜去极化。事实上，向细胞培养物中添加 N-乙酰半胱氨酸可以减轻 Pyr2 enV(IV)诱导的细胞凋亡。这些结果揭示了 Pyr2 enV(IV)的促凋亡活性及其机制，依赖于细胞内 ROS 的增加。