Research: GHOSH,

Listed in Issue 100

Abstract

GHOSH, Department of Urology, Vattikuti Urology Institute, Henry Ford Health System, Detroit, MI 48202, USA, jghosh1@fhs.org, has found that the induction of cell death by selenium in prostate cancer can be reversed by metabolites of the enzyme lipoxygenase.

Background

Clinical trials have shown that selenium significantly reduces the incidence of prostate cancer. The underlying mechanisms by which this happens are not very clear. This paper provides evidence that selenium rapidly induces apoptosis, or programmed cell death, in prostate cancer cells but not in normal prostate cells. Apoptosis involves the activation of an enzyme called cascase 3

Methodology

Biochemical in vitro study.

Results

It was shown that the induction of apoptosis by selenium could be substantially alleviated by the 5-lipoxygenase metabolites 5-HETE and 5-oxoETE, but not by the metabolites of 12-lipoxygenase or 15-lipoxygenase. Apoptosis is also prevented by the precursor of these metabolites, arachidonic acid. Arachidonic acid is an n-6 polyunsaturated fatty acid.

Conclusion

These results suggest that selenium may be a protectant against prostate cancer by acting on cancer cells, but not normal cells, by inducing programmed cell death. They further indicate that care should be taken to avoid high intake of foods or supplements containing arachidonic acid as this may reverse the beneficial effects of selenium. A combination of selenium and 5-lipoxygenase inhibitors may be a better protection against prostate cancer.

References

Ghosh J. Rapid induction of apoptosis in prostate cancer cells by selenium: reversal by metabolites of arachidonate 5-lipoxygenase. Biochemical and Biophysical Research Communications 315 (3): 624-635, Mar 2004.

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