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首页> 外文期刊>Journal of Cellular Physiology >Therapeutic potential of a pyridoxal-based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells
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Therapeutic potential of a pyridoxal-based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells

机译:pyridoxal-based的治疗潜力钒(IV)复杂的选择性为癌症和健康细胞细胞毒性

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摘要

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 (Pyr2enV(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 Pyr2enV(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 Pyr2enV(IV)-induced apoptosis. These results disclose the pro-apoptotic activity of Pyr2enV(IV) and its mechanism, relying on intracellular ROS increase.
机译:钒化合物能起到抗癌作用,部分原因是抑制酪氨酸磷酸酶。(四)复杂(Pyr2enV (IV)),诱导和93%黑色素瘤A375细胞死亡率的57%(人类)和人类肺癌A549细胞,分别;癌症细胞系和人类正常的表皮角化细胞、肺癌细胞和外周血单核细胞。效果依赖于细胞凋亡诱导;引发活性氧增加,紧随其后线粒体膜去极化。n -乙酰半胱氨酸的细胞文化减弱Pyr2enV (IV)全身的细胞凋亡。这些结果披露pro-apoptotic活动Pyr2enV (IV)及其机制,依赖细胞内ROS增加。

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