BIOL 43 |
| Experimental and epidemiological studies indicate that selenium compounds have chemopreventive activity. Induction of apoptosis and inhibition of cell proliferation have been suggested as important cellular events involved in the chemopreventive actions of these compounds. Because agents that disrupt microtubule formation are known to initiate apoptosis, the current study examined the effect of various selenium compounds on in vitro microtubule polymerization. The compounds examined in this study were sodium selenite, L-selenomethionine, Se-methylselenocysteine, benzylselenocyanate(BSC), 4-methoxybenzylselenocyanate (p-methoxyBSC), 4-phenylenebis(methylene)selenocyanate (p-XSC), 2-phenylenebis(methylene)selenocyanate (o-XSC), and 3-phenylenebis(methylene)selenocyanate (m-XSC). All of the selenium compounds, except L-selenomethionine and Se-methylselenocysteine, exhibited a concentration dependent inhibition of microtubule polymerization. The IC50's (µM) for sodium selenite, BSC, p-methoxy-BSC, p-XSC, o-XSC, and m-XSC were 12.0 ± 0.65, 19.5 ± 1.2, 25.3 ± 1.8, 23.5 ± 0.3, 35.7 ± 0.64, and 32.3 ± 1.3, respectively. L-selenomethionine and Se-methylselenocysteine exhibited IC50's greater than 300 µM. Colchicine, under the same experimental conditions, had an IC50 of 1.49 ± 0.08. This study indicates that tubulin/microtubules may be a cellular target for some selenium compounds. This interaction may be involved in the induction of apoptosis associated with these compounds. This study also supports that different chemical forms of selenium can have different biological effects. |
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Frontiers in Chemical Biology
5:00 PM-7:00 PM, Sunday, August 19, 2007 BCEC -- Exhibit Hall - B2, Poster
Division of Biological Chemistry |