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PubMed1999

Selenium compounds inhibit the biological activity of blood platelets.

The action of inorganic forms of selenium (Se) on blood platelet aggregation, secretion and the arachidonate pathway in vitro was studied. It was shown that sodium selenite, after 30 min preincubation, inhibited platelet aggregation induced by 0.1 U/ml of thrombin and by 10 microM ADP (about 30% inhibition of aggregation after pretreatment of platelets with 10(-4) M of Se). Contrary to sodium selenite, sodium selenate did not affect the platelet aggregation induced by either agonist. Pretreatment of blood platelets with sodium selenite resulted in a statistically significant decrease in adenine nucleotide secretion ( P < 0.01) and release of malonyldialdehyde (MDA), produced in equal amounts to TXA(2) , in thrombin-stimulated platelets ( P <0.001). However, selenite did not change the level of MDA/TXA(2) in sodium arachidonate-stimulated platelets. We conclude that the inhibitory effects of sodium selenite on platelet activation could be the result of decreased synthesis and release of secondary agonists (TXA(2), ADP) in stimulated platelets. It is also possible that sodium selenite blocks the release of arachidonic acid from platelet membranes via phospholipases.

Journal Article↗
PubMed1997

Naturally occurring selenium compounds in cancer chemoprevention trials: a workshop summary.

Evidence from epidemiological studies and a human intervention trial indicates that selenium (Se) may have chemopreventive activity in humans. This report summarizes a workshop held by the National Cancer Institute to address the use of naturally occurring Se compounds in future cancer chemoprevention trials. Differences in the metabolism of inorganic and organic Se compounds can be seen both in the biochemical handling of these forms and in their kinetics in humans. Long-term supplementation could result in greater increases in muscle stores for organic rather than inorganic forms. Because of long half-lives, trials may have to be of long duration to assess efficacy and safety. The optimal size of dose for supplementation is controversial with respect to both efficacy and safety. In China, selenosis was observed in some individuals with a sustained intake of at least 750 micrograms/day but was not observed among others with intakes exceeding 1 mg. These levels exceed the reference dose, a measure of the maximal safe intake, which is 350 micrograms/day. A large-scale Se human intervention trial in the United States suggests no harm due to long-term Se intake of more than 200 micrograms/day. Se deficiency has been shown to have deleterious effects on the immune system, allowing, for example, a benign form of the Coxsackievirus to become virulent in mice. These recent results may provide an explanation of earlier findings showing a protective effect of elevated Se intakes against a mouse mammary tumor virus. Additional studies on the use of Se as a chemopreventive agent in man seem warranted.

Animals↗
PubMed2003

Effects of selenium compounds on induction of DNA damage by broadband ultraviolet radiation in human keratinocytes.

Background Ultraviolet radiation (UVR), a ubiquitous environmental genotoxin for the skin, produces DNA damage. The trace element selenium induces synthesis of the glutathione peroxidase and thioredoxin reductase enzyme families. These selenoenzymes detoxify a range of toxic compounds generated by free radicals. Objectives To assess the effects of pretreatment of primary human keratinocytes with selenium on UVR-induced DNA damage. Methods Cells were irradiated with UVR from FS-20 lamps and were subjected to comet assay. Results Comet tail length due to UVR-induced T4 endonuclease V-sensitive sites (caused by cyclopyrimidine dimers, CPDs) increased to 35 +/- 4.5 microm (mean +/- SD) immediately after irradiation (time 0 h, 100%). After 4 h, 68% of the damage remained and after 24 h, 23% of the damage was still present. Treatment with up to 200 nmol L-1 selenomethionine or 50 nmol L-1 sodium selenite had no effect on CPD formation or rates of repair, or on the number of excision repair sites as measured by cytosine arabino furanoside and hydroxyurea treatment. However, selenite and selenomethionine protected against oxidative damage to DNA as measured by formation of formamidopyrimidine (FaPy) glycosylase-sensitive sites, which are indicative of 8-hydroxy-2-deoxyguanosine photoproduct formation. In this assay, irradiation of keratinocytes increased mean +/- SD glycosylase-specific comet tail length from 5 +/- 1.5 microm to 19 +/- 3.3 microm. Preincubation for 18 h with 50 nmol L-1 selenite abolished the UVR-induced increase in comet length. Preincubation with 200 nmol L-1 selenomethionine was similarly protective. Conclusions Selenite and selenomethionine protect keratinocytes from UVR-induced oxidative damage, but not from formation of UVR-induced excision repair sites.

8-Hydroxy-2'-Deoxyguanosine↗
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↗
PubMed2001

Enhanced sensitivity of human oral carcinomas to induction of apoptosis by selenium compounds: involvement of mitogen-activated protein kinase and Fas pathways.

Prospective studies and recent intervention trials suggest that the risk of some cancers, including respiratory tract cancers, may be inversely related to selenium (SE) intake, and this is supported by strong experimental evidence with chemical-induced animal cancer models. How this cancer-protective effect is mediated is unclear, but interference with the balance of growth/apoptosis during tumor outgrowth is one plausible hypothesis. In general, there is a correlation between the effectiveness of SE compounds as chemopreventive agents in vivo and their ability to inhibit cell growth and induce apoptosis in vitro. This study has investigated the signal transduction pathways affected by SE compounds in biopsies of normal human oral mucosa cells and human oral squamous carcinoma cells (SCCs), using a primary culture system. Two SE compounds were tested: selenodiglutathione (SDG), the primary metabolite of selenite and the most commonly used cancer-protective SE compound in animal models, and the synthetic SE compound, 1,4-phenylenebis(methylene)selenocyanate (p-XSC), one of the most potent chemopreventive pharmacological SE compounds. Three novel findings are reported: (a) SCCs were found to be significantly more sensitive to induction of apo ptosis by SDG than normal human oral mucosa cells, though the differences were marginal with p-XSC; (b) both SE compounds induced the expression of Fas ligand (Fas-L) in oral cells to a degree that correlated with the extent of apoptosis induction; and (c) both SDG and p-XSC induced the stress pathway kinases, Jun NH2-terminal kinase (JNK) and p38 kinase, at concentrations causing apoptosis; p-XSC, and to a lesser extent SDG, also activated extracellular regulated kinases 1&2 (ERKs 1&2) and protein kinase-B or Akt. To test their functional involvement, the effect of inhibiting each of these pathways on induction of apoptosis by SDG and p-XSC was determined in SCCs. Inhibiting the ERKs 1&2 or Akt pathways with specific chemical inhibitors (PD98059 or LY294002, respectively) did not affect the extent of apoptosis induced by SDG or p-XSC (with the exception of LY294002, which actually enhanced the level of induction of apoptosis by SDG). The JNK pathway appeared to be most important for induction of Fas-L and apoptosis because concentrations of SB202190 that inhibited activation of both the JNK and p38 kinase (but not ERKs 1&2) in SCC reduced the extent of induction of Fas-L and apoptosis by SDG and p-XSC, whereas lower concentrations that inhibited activation only of p38 kinase did not. This was confirmed by the fact that exogenous expression of a dominant negative deletion mutant of c-Jun (TAM67) reduced the induction of both apoptosis and Fas-L by SDG.

3T3 Cells↗