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EnglishVanadium 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.
| Titolo: | Therapeutic potential of a pyridoxal-based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells |
| Autori: | |
| Data di pubblicazione: | 2013 |
| Rivista: | |
| 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 (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. |
| Handle: | http://hdl.handle.net/11386/4042053 |
| Appare nelle tipologie: | 1.1.2 Articolo su rivista con ISSN |
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