Present research efforts are primarily focused on the mechanism of cancer reduction by selenium, and tissue cultures have been used advantageously to study how tumors are reduced by this element. Research with mouse mammary epithelial cells indicate that the beta-lyase mediated production of a monomethylated selenium metabolite, namely, methylselenol, from SeMCYS is a key step in cancer chemoprevention by this agent.78 In order for SeMCYS to be effective, cells must possess this beta-lyase. One way to get around this is to use methyl-selenenic acid, which is even effective in cells without this lyase. Apparently, mouse mammary epithelial cells have low levels of the beta-lyase. Interestingly, the distinction between these two compounds disappears in vivo where their cancer chemopreventive efficacies were found to be very similar. The reason for this is that the beta-lyase enzyme is abundant in many tissues and thus the animal has ample capacity to convert SeMCYS to methylselenol.
Further work with these mammary cells using methylselenenic acid produced similar results, providing additional support that monomethylated forms of selenium are the critical effector molecules in selenium-mediated growth inhibition in vitro.79 Further research is needed to identify why a monomethylated form of selenium is required, whereas other forms of selenium cannot fulfill this effect. SeMCYS was shown to induce apoptosis through caspase activation in human promyelocytic leukemia cells.80 Moreover, SeMYCS increased both the apoptotic cleavage of poly (ADP-ribose) polymerase and caspase-3 activity, whereas selen-ite did not, indicating specific effects of various selenocompounds.
In other research, selenium was shown to significantly downregulate the expression of prostate-specific antigen transcript and protein within hours in the androgen-responsive cells.81 Selenium also suppressed the binding of androgen receptor to the androgen responsive element site, as shown by electrophoretic mobility shift assay of the androgen receptor-androgen responsive element complex. In further work from this laboratory, exposure to sub-apoptotic concentration of methylseleninic acid specifically inhibited prostate specific antigen expression in the androgen-responsive LNCaP prostate cancer cell model.82 Interestingly, selenite and Semet lacked this inhibitory effect. Work from another laboratory indicated that the use of the recombinant enzyme methioninase, methylselenol-generating chemiluminescence by superoxide was shown to be catalytically produced from Semet, selenoethionine but not from methionine or SeMYCS. It was concluded that methylselenol can be produced from other sources in addition to the action of beta lyase upon SeMYCS.83
As prostate cancer is the most common cancer diagnosed and the second leading cause of cancer-related deaths in men in the U.S.,84 obviously any research to reduce the incidence of this cancer has significant implications. With the use of the H520 and H522 human lung cancer cell lines, methylseleninic acid was shown to inhibit cell growth, arrested cell cycle progression, and induced apop-tosis as a late event.85
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