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PubMed1975

Biological potency of organic selenium compounds: VI. Aliphatic seleninic acids and carboxyselenic acids.

Straight-chain aliphatic seleninic acids, CH3-(CH2)n-SeOOH, with chain lengths from C4 to C17, a few dibasic acids of moderate chain length having seleninic acid groups on both ends of the molecule, HOOSe-(CH2)n-SeOOH, and a series of carbosyseleninic acids, HOOC-R-SeOOH, comprising chain lengths from C3 to C13 and several branched chains with 5 to 7 carbon atoms were tested for potency in the prevention of dietary liver necrosis in the rat. Alkylseleninic acids showed uniformly low activities, ranging from 18% to 56% of that of selenite selenium which served as a standard. There were no discernible trends or regularities with increasing chain lengths, in c-ntrast to other series of alkylselenium compounds. It is therefore unlikely that alkylseleninic acids are normal oxidation products of dialkyl mono- or diselenides in the organism. Compounds with seleninic acid groups at both ends of the chain were practically inactive. Carboxyseleninic acids carrying a carboxyl group distal to the seleninic acid group, on the other hand, were highly effective. A maximum of potency occurred at chain lengths C3 and C4, followed by a sharp decline between C4 and C6. A second maximum of activity occurred at C8. There was no alternating effect. This structure/activity pattern is analogous to that of the diselenodicarboxylic acids. However, the lower carboxyseleninic acids were, per atom of selenium, twice as active as the corresponding diseleno-dicarboxylic acids, of which the higher members were less potent. It is inferred that carboxyseleninic acids may be metabolically related to diseleno-dicarboxylic acids and that C3 and C4 carboxyseleninic acids may play a physiological role.

Animals↗
PubMed1984

Differential effects of sodium selenite and methylmercury(II) on membrane permeability and DNA replication in HeLa S3 carcinoma cells: a preliminary report regarding the modification of organomercurial toxicity by selenium compounds.

When viewed in terms of their concentration in the growth medium, sodium selenite and methylmercuric hydroxide--administered individually to HeLa S3 cells--are of equal efficacy in inhibiting DNA synthesis: the dose-response curves overlap and 50% residual DNA synthesis occurs at 6.13 microM of either chemical. A different picture, however, emerges if replication is expressed as a function of the actual amounts of toxicant bound per cell. Now, the dose-response curves do not overlap and Na2SeO3 is much more toxic than CH3HgOH: 50% inhibition of DNA replication exists at 5.37 X 10(-17) moles of Se bound per cell and at 3.63 X 10(-15) moles of Hg bound per cell. Further, selenite is taken up by the cells more slowly than methylmercury and its (limiting) cellular concentration is below that of the organomercurial. Lastly, much higher levels of selenite in the growth medium are required to bring about the same degree of membrane damage as the one caused by methylmercury. These differential effects may have a bearing on the observation, well-known but thus far unexplained, that selenite and methylmercury are strikingly less toxic to animals when administered simultaneously than they are when administered individually: selenium may counteract the membrane-destabilizing characteristics of methylmercury and it may retard its binding to the cells. Data on the inhibition of DNA synthesis have been obtained when selenite and methylmercury are administered simultaneously to HeLa S3 cells in varied molar ratios. Best mutual protection appears to exist when the two chemicals are present in equimolar amounts or when there is a slight excess of selenite.

Cell Membrane Permeability↗