Selenium supplementation has been shown for many years to work as an anticarcinogenic agent both in epidemiology and in in vitro studies.
Selenium supplementation has recently been shown to decrease total
cancer incidence. However, the mechanism of action of
selenium as an anticarcinogenic agent has yet to be elucidated.
Selenomethionine was the predominant form of
selenium in the dietary supplement in the study by Clark et al. (Clark, L.C., Combs, G.F., Turnbull, W.B., Slate, E.H., Chalker, D.K., Chow, J., Davis, L.S., Glover, R.A., Graham, G.F., Gross, E.G., Krongrad, A., Lesher, J.L., Park, H.K., Sanders, B.B., Smith, C.L., Taylor, J.R. and The Nutritional Prevention of
Cancer Study Group (1996) Effects of
selenium supplementation for
cancer prevention in patients with
carcinoma of the skin: a randomized controlled trial. J. Am. Med. Assoc., 276 (24), 1957-1963) and therefore we evaluated the growth inhibitory effects of
selenomethionine against human
tumor cells.
Selenomethionine was tested against each of three human tumor cell lines (MCF-7/S
breast carcinoma, DU-145
prostate cancer cells and UACC-375
melanoma) and against normal human diploid fibroblasts. All cell lines demonstrated a dose-dependent manner of growth inhibition by
selenomethionine.
Selenomethionine inhibited the growth of all of the human tumor cell lines in the micromolar (microM) range (ranging from 45 to 130 microM) while growth inhibition of normal diploid fibroblasts required 1 mM
selenomethionine, approximately 1000-fold higher than for the
cancer cell lines. In short, normal diploid fibroblasts were less sensitive than the
cancer cell lines to the growth inhibitory effects of
selenomethionine. Furthermore, we show that
selenomethionine administration to these
cancer cell lines results in apoptotic cell death and aberrant mitoses. These results demonstrate the differential sensitivity of
tumor cells and normal cells to
selenomethionine.