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.
Therapeutic potential of a pyridoxal-based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells
STRIANESE, MARIA;BASILE, ANNA;MORELLO, SILVANA;TURCO, Maria Caterina;PELLECCHIA, Claudio
2013
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
