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PubMed1996

Effect of selenium on selenoprotein P expression in cultured liver cells.

Selenoprotein P and glutathione peroxidase are selenoproteins that are synthesized by hepatocytes. The production of these selenoproteins by human and rat liver cell lines has been assessed at several levels of selenium supplementation and compared with one another. HepG2 and H4IIE cells were cultured in serum-free medium without selenium supplementation for 48 h; then sodium selenite was added to the medium to give final concentrations of 0, 1, 2.5, 5, or 10 ng selenium/ml medium. After 48 h, selenoprotein P concentration in the medium, cellular glutathione peroxidase activity, and the mRNA levels of the two selenoproteins were determined. Selenium deficiency caused a decrease in selenoprotein mRNA and protein levels. The extent of decrease depended on the cell line examined. In selenium-deprived HepG2 cells, selenoprotein P release decreased to 10% of the release by selenium-replete cells. Under the same conditions, cellular glutathione peroxidase activity decreased to 33%. H4IIE cells showed the opposite results with cellular glutathione peroxidase activity decreasing to 13% and selenoprotein P release decreasing to 40% of selenium-replete cells. The effect of dithiothreitol on secretion of selenoprotein P by H4IIE cells was examined. Selenoprotein P secretion was inhibited by dithiothreitol, suggesting that disulfide bond formation is necessary for secretion of the mature protein.

Animals↗
PubMed1984

A comparison of the effect of selenium on the mutagenicity and metabolism of benzo[a]pyrene in rat and hamster liver S9 activation systems.

When selenium (Na2SeO3) was included in the incubation mix containing rat or hamster liver S9 preparations both the metabolism and mutagenicity of benzo[a]pyrene (BaP) and several of its metabolites were altered. At non-toxic concentrations selenium inhibited the S9 dependent mutagenicity of BaP and a number of its metabolites on Salmonella typhimurium strain TA100 as indicated by the number of histidine independent revertants observed. High performance liquid chromatographic analysis of S9 generated metabolites of BaP from rat and hamster liver indicated that selenium caused quantitative differences in the amounts of the metabolic products. In hamster liver S9 differences were reflected in decreased amounts of strongly mutagenic BaP-7,8-dihydrodiol and increased amounts of 4,5- and 9,10-dihydrodiols that were weakly mutagenic to TA100 in that system. In rat liver S9 selenium caused quantitatively similar decreases in BaP-7,8- and 9,10-dihydrodiol and 3-hydroxy-BaP. When used as substrate 3-hydroxy-BaP was the most mutagenic to TA100 in the rat activation system whereas BaP-7,8-dihydrodiol was most mutagenic in the hamster S9 system. Assays that measured the formation of water-soluble conjugates of BaP indicated that selenium did not significantly alter the formation of sulfate ester or glutathione conjugates although a 12-17% reduction of labeled metabolites bound to the glucuronide fraction was observed. Results described in this report suggest that selenium modified the metabolism and hence the mutagenicity of BaP to TA100 by affecting mixed-function oxidase and/or epoxide hydratase activity in both the rat and hamster liver S9 activation systems.

Animals↗
PubMed1984

Selenium inhibition of the neoplastic transformation in preneoplastic mammary cell populations.

The effect of dietary selenium on the tumor-producing capabilities of primary hyperplastic alveolar nodules (HAN) of the mammary gland of BALB/c mice was examined directly using a transplantation assay. The tumor-producing capabilities of primary HAN exposed to 2.0 ppm dietary selenium was decreased 57% compared to the tumor-producing capabilities of HAN exposed to 0.2 ppm dietary selenium. This degree of inhibition compared well with the 60% inhibition of mammary tumorigenesis when the mice were exposed to supplemental selenium during the entire tumorigenic period. The examination of primary hyperplastic alveolar nodules was a more accurate assessment of the responsiveness of the preneoplastic state than using established nodule outgrowth lines since the latter exhibited a greater degree of variability in response to selenium-mediated inhibition of growth and the mean response of numerous nodule outgrowth lines was not as great as seen in the primary HAN. These results indicate that selenium is an effective inhibitor of the neoplastic transformation in preneoplastic cells as well as the formation of preneoplastic cells.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

A selenocysteine-containing selenium-transport protein in rat plasma.

A selenocysteine-containing rat plasma protein (selenoprotein P) was examined for a possible role in the transport of selenium in the rat. A time-course study of the localization of injected 75Se from [75Se]selenite indicated that one-half of the selenium was sequestered by liver tissue 1 h after injection and that one-fourth of the 75Se in the plasma was attached to selenoprotein P 3 h after injections. By 25 h there was little 75Se in plasma, and much of the 75Se had accumulated in nonhepatic tissues. 75Se was incorporated into selenoprotein P by liver slices in a process that was sensitive to the protein synthesis inhibitor cycloheximide. The fate of 75Se from intracardially injected 75Se-labeled selenoprotein P was followed in rats maintained on selenium-deficient and selenium-sufficient diets. Substantially more of the injected 75Se was present per gram wet weight in the testes and kidneys than the livers of the selenium-deprived rats after 5 h. The results indicate that selenoprotein P is synthesized in rat liver and that it transfers selenium from the liver to extrahepatic tissues.

Animals↗
PubMed1987

Influence of selenium deficiency on glutathione disulfide metabolism in isolated perfused rat heart.

Selenium deficiency causes a fall in rat cardiac glutathione peroxidase activity. As a consequence, isolated perfused selenium-deficient heart does not release increased amounts of GSSG when hydroperoxide is infused. However, the total amount of glutathione measured as intracellular GSH, intracellular GSSG and GSSG released from the heart when hydroperoxide is infused does not equal the total glutathione measured in these pools in untreated hearts (Xia, Y., Hill, K.E. and Burk, R.F. (1985) J. Nutr. 115, 733-742). GSSG can react with protein sulfhydryl groups to form glutathione-protein mixed disulfides (PrS-SG). PrS-SG were measured in perfused selenium-deficient and control hearts infused with t-butylhydroperoxide and were found to account for the previously unmeasured glutathione. The ability of the selenium-deficient heart to transport GSSG was also examined. GSSG was produced non-enzymatically by infusing diamide. The diamide-treated selenium-deficient heart formed GSSG and released it at the same rate as similarly-treated control heart. Thus although selenium deficiency decreases GSSG formation by glutathione peroxidase, it does not affect cardiac GSSG transport.

Animals↗
PubMed1988

Has selenium a beneficial role in human exposure to inorganic mercury?

Laboratory experiments have indicated that selenium acts as a powerful antagonist to mercury intoxication. The literature is reviewed and from this it is concluded that mercury and selenium react in various ways. 1) The mercuric ion binds to selenium to form a biologically inert complex leading to increased body burden of both elements. This reaction seems to take place only when a threshold of mercury exposure is exceeded. 2) Selenium influences the oxidation rate of elemental mercury and as such the distribution pattern. This reaction is influenced by the nature of the antioxidative system. In species with low glutathione peroxidase activity, mercury oxidation seems decreased which can lead to an increased brain uptake. In this process there is no threshold. 3) Selenium can, as part of the antioxidative defence system, counteract mercury induced lipid peroxidation. Other antioxidants e.g. vitamin E might be just as effective. Based upon the literature it is hypothesised that to man selenium is of no benefit in cases of exposure to mercury either as mercuric mercury or as vapours. The only protection against mercury will still be a low exposure level.

Free Radicals↗
PubMed2005

Comparative excretion and tissue distribution of selenium in mice and rats following treatment with the chemopreventive agent 1,4-phenylenebis(methylene)selenocyanate.

In a previous preliminary investigation, we reported on the excretion, tissue disposition and metabolism of the chemopreventive agent 1,4-phenylenebis(methylene)selenocyanate (p-XSC) in the rat, but similar studies in the mouse have not been explored. Following the oral administration of p-XSC (50 micromol/kg body weight), selenium excretion in feces was comparable to that in urine in mice, but in rats, feces was the major route of excretion. Tetraselenocyclophane (TSC) was the major metabolite detected in mouse and rat feces. In both species, levels of selenium in exhaled air were negligible. At termination, in the mouse, the stomach had the highest selenium content followed by liver and blood, but lung and kidney contained negligible levels of selenium; in the rat, the selenium level in liver was the highest followed by kidney, stomach, blood and lung. The identification of TSC as a fecal metabolite in both species let us to postulate the following metabolic pathway: p-XSC-->glutathione conjugate (p-XSeSG)-->a selenol (p-XSeH)-->TSC. Since the glutathione conjugate appears to be the proximal precursor for the selenol metabolite that may be an important intermediate in cancer chemoprevention, we report for the first time the synthesis of p-XSeSG and its other potential metabolites, namely the cysteine- and N-acetylcysteine-conjugates of p-XSC. HPLC analysis of the urine and bile showed a few metabolites of p-XSC; none of which eluted with the synthetic standards described above. When we examined the conversion of p-XSC and p-XSeSG in vitro using rat cecal microflora, TSC was formed from p-XSeSG but not from p-XSC. The formation of TSC from p-XSC in vivo but not in vitro suggests that p-XSC needs to be metabolized to p-XSeSG or an intermediate derived from its further metabolism. Thus, p-XSeSG was given orally to rats and the results showed that the pattern of selenium excretion after p-XSeSG treatment was similar to that of p-XSC; TSC was also identified as a fecal metabolite of p-XSeSG. It may be that the conversion of p-XSeSG to TSC is too facile, or the mere conjugation of p-XSC with glutathione does not occur in rats and mice.

Animals↗
PubMed2006

Two fatal cases of selenium toxicity.

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.

Abdominal Pain↗
PubMed2006

Effect of mercury on selenium utilization and selenoperoxidase activity in LNCaP cells.

Formation of stable complexes with protein thiols is the best-known mechanism of mercury toxicity. However, the solubility product of Hg(2+) with sulfides, although very low, is higher than that with selenides, suggesting that the fully reduced form of selenium might also be a relevant target for Hg(2+). In cells, selenide is the suggested intermediate for selenoprotein biosynthesis and selenoenzymes, in turn, contain reduced selenium as the catalytic moiety. Thus, inhibition of biological functions of selenium could be seen as a different mechanism of Hg(2+) toxicity. To address this issue, we investigated selenoperoxidase (SeGPx) activity in LNCaP cells exposed to HgCl(2). Cells growing in standard medium express a low GPx activity, which increases on addition of selenium donors such as selenite, selenomethionine, or methyl-Se-cysteine. HgCl(2) added to the medium has different effects depending on the type of Se donor. A progressive decrease of SeGPx activity is observed in cells grown in standard medium exposed to HgCl(2), while coadministration of suprastoichiometric amounts of HgCl(2) prevents the increase of SeGPx activity only when selenite, but not selenomethionine or methyl-Se-cysteine, is the selenium source. From this evidence we conclude that HgCl(2): (a) does not inhibit directly SeGPxs, as confirmed on isolated enzymes; (b) does not interfere with the intermediates of the metabolic pathway of selenoprotein synthesis; and (c) decreases the bioavailability of selenium only when ionic complexes can be formed.

Humans↗
PubMed2004

Effects of dietary selenium on glutathione peroxidase and thioredoxin reductase activity and recovery from cardiac ischemia-reperfusion.

Glutathione peroxidase and thioredoxin reductase are selenocysteine-dependent enzymes that protect against oxidative injury. This study examined the effects of dietary selenium on the activity of these two enzymes in rats, and investigated the ability of selenium to modulate myocardial function post ischemia-reperfusion. Male wistar rats were fed diets containing 0, 50, 240 and 1000 microg/kg sodium selenite for 5 weeks. Langendorff perfused hearts isolated from these rats were subjected to 22.5 min global ischemia and 45 min reperfusion, with functional recovery assessed. Liver samples were collected at the time of sacrifice, and heart and liver tissues assayed for thioredoxin reductase and glutathione peroxidase activity. Selenium deficiency reduced the activity of both glutathione peroxidase and thioredoxin reductase systemically. Hearts from selenium deficient animals were more susceptible to ischemia-reperfusion injury when compared to normal controls (38% recovery of rate pressure product (RPP) vs. 47% recovery of RPP). Selenium supplementation increased the endogenous activity of thioredoxin reductase and glutathione peroxidase and resulted in improved recovery of cardiac function post ischemia reperfusion (57% recovery of RPP). Endogenous activity of glutathione peroxidase and thioredoxin reductase is dependent on an adequate supply of the micronutrient selenium. Reduced activity of these antioxidant enzymes is associated with significant reductions in myocardial function post ischemia-reperfusion.

Animals↗
PubMed2006

Effects of selenium supplementation on expression of glutathione peroxidase isoforms in cultured human lung adenocarcinoma cell lines.

Selenium is an essential nutrient, a component of several anti-oxidant enzymes, and a possible factor in cancer risk, including lung cancer. We determined the subtoxic range of selenium concentration (as sodium selenite) required to increase and maintain the expression of anti-oxidant selenoproteins gluthathione peroxidases GPX1 and GPX4 at a constant level in cultures of human lung adenocarcinoma cell lines (H460, H1703 and H1944) and in HPL1D, a non-transformed lung epithelial cell line. Selenium dose-dependently increased GPX1 protein expression 1.8-fold in HPL1D cells and approximately 40-fold in H460 and H1944 cancer cells, with maximum effects at 20-40 nM. GPX4 protein was also increased, but more so in HPL1D (five-fold) than in H460 or H1944 cells (two- to three-fold). GPX1 mRNA showed similar patterns but differences of lesser magnitude. GPX1 protein and activity level was not consistently detectable in H1703 cells, with or without Se supplementation; its mRNA was present but very low. GPX4 protein level was also low in H1703 cells, but was markedly increased by selenium supplementation (48-fold). These results confirm a role for selenium in risk of lung cancer and the independent regulation of GPX1 and GPX4. Characterization of individual tumors with regard to GPX1 and GPX4 levels and regulation might be useful for interpretation of clinical studies on effects of selenium in lung cancer risk.

Adenocarcinoma↗
PubMed2004

Does selenium deficiency unmask mercury toxicity in motor neurons?

OBJECTIVE: Inorganic mercury enters in particular motor neurons and has been implicated in motor neuron diseases. One way that cells protect themselves from mercury toxicity is via selenium, so we sought to determine whether the motor neurons of mice on a low selenium diet would be more susceptible to mercury toxicity. METHODS: Recently weaned mouse pups were placed on diets containing either low, normal or high levels of selenium. Twenty days later, half were exposed to mercury vapor. Ninety days after exposure, their spinal motor neurons and phrenic motor axons were examined histologically. Mercury in the spinal cord was sought using autometallography. RESULTS: Neither low nor high selenium diets combined with mercury vapor had any clinical effect on the mice. Mercury was seen within the spinal motor neurons of all exposed mice. Spinal motor neurons and phrenic motor axons however appeared normal in morphology and size across the groups. CONCLUSION: Diets low or high in selenium did not damage motor neurons with or without mercury. This suggests that changes in the selenium environment are unlikely to precipitate mercury toxicity in motor neurons.

Animals↗
PubMed2006

Selenium supplementation, soluble tumor necrosis factor-alpha receptor type 1, and C-reactive protein during psoriasis therapy with narrowband ultraviolet B.

OBJECTIVE: We examined the influence of supplementation with selenomethionine on soluble tumor necrosis factor-alpha receptor type 1 (sTNF-R1) and C-reactive protein (CRP) concentrations in patients with psoriasis who were treated with narrowband ultraviolet B. METHODS: Thirty-seven patients had narrowband ultraviolet B therapy five times a week and received 200 mug of selenium daily as selenomethionine (group 1, n = 19) or placebo (group 2, n = 18) for 4 wk. Assessment, performed at baseline, after 2 and 4 wk, and 4 wk after the end of treatment included measurement of the Psoriasis Area and Severity Index (PASI) and serum concentrations of selenium (micrograms per liter), sTNF-R1 (nanograms per milliliter), and CRP (milligrams per liter). Control sera were obtained from 20 healthy volunteers. RESULTS: Baseline PASI was 12.70 +/- 5.48 (13.02 +/- 6.25 in group 1 and 12.37 +/- 4.71 in group 2), selenium concentration was 50.55 +/- 9.54 (49.05 +/- 10.38 and 52.13 +/- 8.61, respectively), sTNF-R1 concentration was 1.91 +/- 0.38 (1.96 +/- 0.37 and 1.87 +/- 0.40, respectively), and CRP concentration was 25.34 +/- 8.27 (26.12 +/- 8.42 and 24.57 +/- 7.72). In controls, selenium concentration was 48.71 +/- 9.39 (P > 0.05 versus patients), sTNF-R1 concentration was 1.48 +/- 0.30 (P < 0.05), CRP concentration was <6. The baseline sTNF-R1 level correlated to PASI value (r = 0.40, P < 0.05) and CRP concentration (r = 0.36, P > 0.05). The treatment resulted in an almost parallel decrease in PASI in both groups. At 4 wk after the end of treatment, selenium concentrations were 83.77 +/- 5.13 in group 1 and 52.12 +/- 7.54 in group 2 (P < 0.05), sTNF-R1 concentrations were 1.72 +/- 0.27 and 1.47 +/- 0.26 (P < 0.05), and CRP concentrations were 7.72 +/- 4.23 and 8.15 +/- 3.32, respectively (P > 0.05). Selenium concentration correlated inversely with CRP in group 1. CONCLUSION: The results confirm that sTNF-R1 and CRP concentrations are increated in active psoriasis and that supplementation with selenomethionine for 4 wk in safe doses is ineffacious as adjuvant therapy in patients with psoriasis.

Administration, Oral↗
PubMed2004

Selenium status in Greenland Inuit.

In Greenland, the human intake of selenium has always been relatively high and is closely connected to intake of the traditional food of marine origin. Analyses of historic and present day human and animal hair samples have indicated that the selenium level in the marine environment has been constant over time, while the levels in humans have declined corresponding to a decrease in intake of traditional food. The Inuit population in Greenland is in dietary transition where western-style food will increasingly dominate. As a consequence, the ample supply of selenium may not be sustained in the future. We report here the selenium status in three Greenlandic population groups, Ittoqqortoormiit and Tasiilaq on the east coast and Uummannaq on the west coast. Mean whole blood concentrations ranged from 178 microg/l in Tasiilaq men to 488 microg/l in Uummannaq men. Plasma concentrations ranged from 79 microg/l in Tasiilaq women to 113 microg/l in Uummannaq men. With increasing Se concentrations in whole blood, the plasma concentrations increased but tended to stabilise a level approximately 140 microg/l. Selenium blood levels were highly significantly correlated with long chain marine fatty acids. Dietary survey and food composition data from the west coast showed that whale skin, muktuk, is the main source of Se followed by birds, seal meat and organs, and fish. Terrestrial animals contributed only insignificantly to the selenium intake. In West Greenland, daily Se intake (235 microg/day) was estimated by dietary survey; it corresponded well with a calculated intake (220 microg/day) based on the mean blood concentration.

Adolescent↗
PubMed2005

Whole blood selenium content in healthy adults in the Czech Republic.

Over a 5-year period, from 1996 to 2001, blood selenium levels were recorded in a set of 2414 healthy blood donors (1781 men and 633 women; 880 smokers and 1534 nonsmokers) living in four selected areas of the Czech Republic. About 100 blood samples per year and region were analyzed using the HGA method. The internal and external quality controls of this method were performed throughout the duration of the study. In general, blood selenium concentrations (81.9 and 106.7 microg/l for median and 90th percentile, respectively) did not reach optimum values; in approximately 10% of the population sample, values lower than 60 microg/l were detected. Nonetheless, the values obtained increased significantly, with median concentrations of 73.2 microg/l in 1996 and 91.5 microg/l in 2001. The percentage of subjects with a whole blood selenium level of less than 60 microg/l also decreased from nearly 20% in 1996 to 0.2% in 2001. No substantial regional or gender-related differences were observed, but significantly lower blood selenium levels were found in smokers as opposed to nonsmokers. Although mild selenium deficiency continues to be observed, the data presented do not indicate extremely low selenium levels in the population sample.

Adult↗
PubMed1977

Cancer mortality correlation studies--III: statistical associations with dietary selenium intakes.

Age-corrected mortalities from cancer at 17 major body sites were correlated with the apparent dietary selenium intakes estimated from food-consumption data in 27 countries. Significant inverse correlations were observed for cancers of large intestine, rectum, prostate, breast, ovary, lung and with leukemia; weak inverse associations were found for cancers of pancreas, skin and bladder. Similar inverse corelations were found between cancer mortalities at the above sites and the selenium concentrations in whole blood collected from healthy human donors in the U.S. and different countries. The results support the hypothesis that selenium has cancer-protecting effects in man. Other studies are cited which demonstrate that selenium prevents or retards tumor development in animals. A change of diet aimed at increasing the dietary selenium supply is suggested as a possible means of lowering the human cancer risk. It is postulated that the cancer mortalities in the U.S. and other Western industrialized nations would decline significantly if the dietary selenium intakes were increased to approximately twice the current average amount supplied by the U.S. diet.

Age Factors↗
PubMed2000

Selenium, an antioxidant, attenuates methamphetamine-induced dopaminergic toxicity and peroxynitrite generation.

Methamphetamine (METH) has been known to produce neurotoxicity via generation of reactive oxygen and nitrogen species. Selenium, an antioxidant, was reported to protect against METH-induced dopaminergic neurotoxicity in mouse caudate nucleus. In the present study, the in vitro and in vivo efficacy of the supplementation of selenium was studied in METH-induced generation of peroxynitrite. PC12 cell cultures were exposed to 200 microM METH either with or without 10 microM and 20 microM selenium (30 min prior to METH exposure). After 24 h, METH exposure resulted in the significant depletion of dopamine, and its metabolites DOPAC and HVA, as well as the significant formation of 3-nitrotyrosine (3-NT), a marker of peroxynitrite generation, in PC12 cell cultures. Selenium supplementation attenuated the depletion of dopamine and its metabolites, DOPAC and HVA and the formation of 3-NT in PC12 cells. For in vivo studies, adult male mice were supplemented with selenium in drinking water, 1 week before and 1 week after the multiple injections of METH (4x10 mg/kg, i.p. at 2-h interval) or an equivalent volume of saline. The supplementation of Se attenuated the formation of 3-NT in the striatum resulting from METH treatment. These data suggest that METH-induced neurotoxicity is mediated by the production of peroxynitrite, and selenium plays a protective role in METH-induced neurotoxicity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

Determination of selenium compounds in urine by high-performance liquid chromatography--inductively coupled plasma mass spectrometry.

Selenium species, selenite, selenate, selenomethionine (Semet), seneloethionine (Seet) and trimethylselenonium ion (TmSe) were separated in aqueous solution using a gel-permeation (polyvinyl alcohol-based resin) GS-220 column by eluting with 25 mM tetramethylammonium hydroxide and 25 mM malonic acid at pH 7.9. The GS-220 column coupled with inductively coupled plasma mass spectrometry was used for the separation, identification, and quantification of selenium compounds present in certified reference material (CRM) No. 18 human urine from the National Institute for Environmental Studies in Japan (NIES). Spiking of the authentic standard to the urine and use of a silica-based LC-SCX cation-exchange column validated the peak of selenium compounds. High concentrations of chloride and bromide in the urine eluted from the GS-220 column formed molecular ions 40Ar37Cl+ and 81Br1H+ in the plasma, and these molecular ions created additional peaks in the chromatograms when 77Se and 82Se isotopes were monitored respectively. Thus, both the isotopes were selected concurrently for signal monitoring to eliminate the interfering signals. On the LC-SCX column, chloride and bromide were eluted with selenate and complicated its determination, but the peak of TmSe was baseline separated from rest of the Se compounds. Two unknown Se compounds were detected in both the columns. An additional Se compound having the same retention time as that of Semet was detected on the LC-SCX column. Peaks of selenite, selenate, TmSe and unknown selenium compounds in the urine were baseline separated on the GS-220 column, and were free from interferences. Therefore, the GS-220 column was used for the determination of selenium compounds in NIES CRM No. 18. Unknown Se compounds were the predominant selenium species followed by selenite, TmSe and selenate. The estimated value of TmSe as Se, by the standard additions method using the GS-220 column, was 3.42 +/- 0.17 microg l(-1) and was in good agreement with the LC-SCX value [3.38 +/- 0.21 (n=5) microg l(-1)].

Cations↗