Therapeutic potential of a pyridoxal‐based vanadium(IV) complex showing selective cytotoxicity for cancer versus healthy cells. Issue 11 (25th July 2013)

• Record Type: Journal Article
• Authors: Strianese, Maria; Basile, Anna; Mazzone, Antonio; Morello, Silvana; Turco, Maria Caterina; Pellecchia, Claudio
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 11(2013:Nov.)
• Page Start: 2202
• Page End: 2209
• Publication Date: 2013-07-25
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24385
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="jcp24385-sec-0001" sec-type="section"> <p>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 &lt;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 <italic>N</italic>‐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. J. Cell. Physiol. 228: 2202–2209, 2013. © 2013 Wiley Periodicals, Inc.</p> </sec> </abstract>