Molybdenum and Cancer
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- Category: Molybdenum knowledge
- Published on 29 March 2013
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The polyoxomolybdate(V) ( PM-17), is prepared by photo-reduction of the heptamolybdate, [NH3Pri]6[MoVI7O24].3H2O (PM-8). It is an anti-tumour agent inhibiting the growth of human pancreatic cancer (AsPC-1) xenografts in a nude mice model, and induced morphological alterations in tumour cells. Correspondingly, PM-17 repressed the proliferation of AsPC-1 cells and human gastric cancer cells (MKN45) depending on the dose in vitro.
It is proposed that PM-8 could be taken preferentially into tumour cells and reduced biologically probably in the mitochondrial system. PM-17 is one of the reduced species of PM-8. The effect of the biological reduction would be to inhibit ATP generation. The reduction product is ca ten-fold more toxic than PM-8. Such a difference in toxicity between PM-8 and its reduced species would lead to a tumour-selective inhibition because (a) the reduced species, on account of its greater molecular weight, would stay longer in the tumour cells (b) the tumour cells exhibit a higher metabolism.
Doses of PM-17 (125 microg and 500 microg per 100 microL 0.9% NaCl solution, per body per day) reduced the growth rate, compared with a control, of AsPC-1 tumour cells implanted in mice over a period of 40 d without affecting the growth rate of the mice. The tumour growth inhibition was greater with the higher PM-17 doses (33.5% and 68.3% after 41 days). Thus PM-17 inhibits the proliferation of AsPC-1 human pancreatic tumours in a dose-dependent manner in vivo.
An account of the possible mechanism of tumour cell death is given. PM-17 induces both apoptosis and autophagy in human pancreatic cancer AsPC-1 cells.Sharp DNA laddering was observed after treatment with PM-17 by agarose gel electrophoresis of cell DNA extracts which fonfirmed the induction of apottosis by PM-17.PM-17 was not toxic to mice; they showed no impaired renal or hepatic function, nor haematocytes nor less of body weight.
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