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PubMed1988

Efficacy of trimethylselenonium versus selenite in cancer chemoprevention and its modulation by arsenite.

Selenite, which has been demonstrated to be an effective prophylactic agent in experimental carcinogenesis, is metabolized to trimethylselenonium as an excretory product. Previous reports in the literature have shown that arsenite decreases the toxicity of selenite but increases that of trimethylselenonium. The present study was designed to compare the anti-carcinogenic efficacy of selenite and trimethylselenonium and their interactions with arsenite in chemoprevention, using the dimethylbenz[a]anthracene-induced mammary tumor model in rats. The results of this experiment indicated that supplementation of selenite (3 p.p.m. Se) alone produced approximately 50% reduction in tumor yield, and arsenite (5 p.p.m. As) reduced the response to selenite. In contrast, arsenite greatly enhanced the protective effect of trimethylselenonium (40 p.p.m. Se); this combination was nearly as effective as selenite, although either trimethylselenonium or arsenite alone was inactive. Thus, arsenite has the capacity to influence the anti-carcinogenic action of selenium, and can either potentiate or attenuate the protective effect depending on the methylation state of the selenium compound. The metabolism of selenium and its perturbation by arsenite are discussed in relation to the above findings.

Animals↗
PubMed1979

The influence of selinium on methyl mercury toxicity in rat hepatoma cells, human embryonic fibroblasts and human lymphocytes in culture.

The effect of methyl mercury and two selenium compounds have been studied in cell cultures. Methyl mercury in concentrations above 1 microM had a pronounced inhibiting effect on the growth of rat Morris hepatoma cells. Glucose and lactate uptake in relation to cell protein was appreciably stimulated by the organic mercury compound. Selenite in low concentration (0.5 microM) and seleno-di-N-acetyl glycine in thousandfold higher concentrations offered considerable protection against these effects of methyl mercury. The same selenite concentration (0.5 microM), which did not affect cell growth, caused an appreciable protection against methyl mercury (6 microM), even if it was added 3 days after methyl mercury. The methyl mercury inhibited the growth of human embryonic fibroblasts and the DNA-synthesis in the human lymphocytes. However, no protective effect of selenite were observed in these cell types. These results suggest that selenium compounds exert their protective effect through cell specific processes rather than by a direct chemical reaction between selenite and methyl mercury.

Animals↗
PubMed1986

Mercury, silver, and gold inhibition of selenium-accelerated cysteine oxidation.

In vivo, cysteine in proteins or glutathione is the major amino acid involved in sulfhydryl oxidation-reduction reactions. An in vitro model of cysteine oxidation accelerated by selenium compounds was used to study the interaction of selenocystine and sodium selenite with metal ions. The interaction of metal ions with selenium compounds inhibited cysteine oxidation. The ionic forms of three toxic soft-acid metals, mercury, silver, and gold, were the most effective inhibitors. The antiarthritic gold drugs, aurothiomalate and aurothioglucose, were of particular interest as they inhibit the activity of selenium-glutathione peroxidase. The effect of gold ligands on gold(I) inhibition of selenocystine-accelerated cysteine oxidation was tested. Sodium cyanide partially reversed inhibition and potassium iodide had no effect. Inhibition of selenium-accelerated oxidation-reduction reactions by soft-acid metal ions may be of biological relevance during toxicities or during antiarthritic gold therapy.

Cysteine↗
PubMed1989

Susceptibility of methicillin-resistant Staphylococcus aureus to the selenium-containing compound 2-phenyl-1,2-benzoisoselenazol-3(2H)-one (PZ51).

The growth of Staphylococcus aureus 209P was inhibited by 0.20 micrograms of 2-phenyl-1,2-benzoisoselenazol-3(2H)-one (PZ51) per ml, while strains of the family Enterobacteriaceae were more resistant to the drug. The MIC for 90% of methicillin-resistant S. aureus strains was 1.56 micrograms/ml, and the drug was bactericidal. The selenium in PZ51 was essential, since its sulfur analog (PZ25) lost the antibacterial activity.

Azoles↗
PubMed1976

Fluoride-selenium interaction in the hard and soft tissues of the rat.

The interaction of dietary fluoride and selenium in the hard and soft tissues of rats was studied by providing drinking solutions containing 50 ppm F, as NaF, alone or plus 1 or 3 ppm Se as one of the following selenium compounds: NaSeO3, Na2SeO4, DL-selenomethionine, or DL-selenocystine. The following parameters were measured: symptoms of selenium toxicity, soft tissue uptake of fluoride and selenium, histology of liver and kidney tissues, fluoride uptake into growing femur bones, and fluoride uptake onto calcified molar enamel. No evidence was found that fluoride interacted with any of the four selenium compounds.

Animals↗
PubMed1991

Changes in ornithine decarboxylase activity and polyamine levels in response to eight different forms of selenium.

The biological activity of selenium is known to depend on its chemical form. In this study, eight forms of selenium that differed in oxidation state or degree of methylation were studied for their acute effects on the activities of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMet DC) and on the concentrations of the polyamines putrescine, spermidine, and spermine in the liver. The polyamine pathway was studied because it is involved in the control of cell growth and in the cell's response to trophic, carcinogenic, and toxic stimuli, activities that selenium has been reported to affect. Female Sprague Dawley rats were administered 12 mumol Se/kg body weight via intraperitoneal injection and were sacrificed six hours later. Injection of sodium selenate, sodium selenite, selenomethionine, Se-methylselenocysteine, selenobetaine, and selenobetaine methyl ester resulted in significant increases in liver selenium, whereas injection of dimethylselenoxide and trimethylselenonium chloride did not. ODC activity and AdoMet DC activity were induced by those selenium compounds that also increased liver selenium content, but the magnitude of enzyme induction by those compounds was not correlated with the hepatic concentration of total selenium determined fluorometrically. Furthermore, the induction of ODC activity by the various forms of selenium did not result in concomitant increases in putrescine, spermidine, and spermine except in the case of selenite. Given that alterations in the metabolism of selenium are induced when the level of tissue selenium is elevated and that the relative abundance of various selenometabolites can be affected by the point of entry of selenium into intermediary metabolism, these data suggest that the changes that were observed in enzyme activities and polyamine levels are likely to be associated with the accumulation of a specific metabolite of selenium. The relevance of these findings to elucidation of the biological activities attributable to various forms of selenium is under investigation.

Adenosylmethionine Decarboxylase↗
PubMed1986

Interaction of vitamin C and selenium supplementation in the modification of mammary carcinogenesis in rats.

The objectives of this study were a) to compare the efficacy of inorganic and organic selenium compounds in protecting against mammary tumorigenesis induced by 7,12-dimethylbenz[a]anthracene [(DMBA); CAS: 57-97-6] in rats and b) to study the interaction of vitamin C with either selenite (inorganic) or seleno-DL-methionine (organic) in chemoprevention. Control Sprague-Dawley rats were fed a purified 5% corn oil diet containing 0.1 ppm selenium. Selenite or seleno-DL-methionine was added to the basal diet in concentrations of 2, 3, or 4 ppm starting 1 week after DMBA administration. The inhibitory response in mammary tumorigenesis with selenium supplementation was dose dependent. Both selenium compounds were found to be equally efficacious in prophylaxis, although at the 4-ppm level a slight reduction in growth was observed. In the second experiment, different concentrations of vitamin C (0.2, 0.5, and 1%) were tested. In general, there was no change with the two lower levels; but a slight, although insignificant, increase in tumor yield was detected in rats supplemented with 1% vitamin C in the diet. The interaction of 0.5% vitamin C with either selenite or seleno-DL-methionine (3 ppm) was studied in the third experiment. Results showed that the protective effect of selenite in tumorigenesis was nullified by vitamin C, whereas the chemopreventive action of seleno-DL-methionine was not affected. It is possible that selenite is reduced by vitamin C to elemental selenium and is therefore not available for uptake by tissues. This hypothesis was indirectly supported by tissue selenium measurements showing that 0.5 or 0.25% of vitamin C in the diet completely negated in blood, liver, and mammary gland the accumulation of selenium induced by 3 ppm of selenite supplementation. Lower levels of vitamin C (less than or equal to 0.1%) were found to have no effect on tissue selenium concentrations. Furthermore, the presence of 0.1% vitamin C in the diet no longer abolished the anticarcinogenic effect of selenite. This study suggests that high levels of vitamin C can interfere with the accumulation of tissue selenium and that an increased titer of this trace element in cells is essential for retarding tumor development.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Selective reduction of cis-diamminedichloroplatinum(II) nephrotoxicity by ebselen.

2-Phenyl-1,2-benzisoselenazol-3(2H)-one (ebselen) is classified as a relatively nontoxic selenium compound, probably because of its bound selenium moiety. In thiol-rich tissues, such as the kidneys, ebselen is converted into selenol intermediates. Selenols are nucleophilic agents which might be able to react with platinum compounds. The influence of ebselen on cis-diamminedichloroplatinum(II) (cisplatin)-induced nephrotoxicity in mice was assessed, using single doses of both compounds. Ebselen prevented cisplatin-induced elevations of blood urea nitrogen and serum creatinine levels and morphological kidney damage in BALB/c mice. This protective effect of ebselen was dose dependent: at a cisplatin dose of 14.5 mg/kg, maximal protection was achieved when a single dose of 10 mg of ebselen/kg was administered 1 h before cisplatin. Administration of ebselen, 10 mg/kg, 1 h after cisplatin also protected against severe nephrotoxicity. Treatment with ebselen did not reduce the antitumor activity of cisplatin against MPC 11 plasmacytoma or Prima breast tumor in BALB/c mice. However, this reduction of cisplatin-induced nephrotoxicity would be of little clinical value if it was achieved at toxic doses of ebselen. Ebselen, 10 mg/kg, did not induce blood urea nitrogen, serum creatinine, serum glutamic pyruvate transaminase, or serum glutamic oxalate elevations in the mice. These results are in agreement with the reported low toxicity of ebselen, which is now in Phase I clinical trials as an antiinflammatory drug. The present results indicate that ebselen may provide protection against cisplatin-induced nephrotoxicity, when it is given before or after cisplatin. This might open new perspectives in cancer chemotherapy.

Animals↗
PubMed1987

Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury.

The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 mumoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 mumoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 mumoles/kg dose levels decreased in the order of no selenium greater than biological selenium greater than seleno-dl-methionine greater than selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 mumoles/kg dose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

X-ray photoelectron spectroscopy of some selenium containing amino acids.

X-ray photoelectron spectra of some inorganic selenium compounds, Se-methionine, Se-cystine, Se-urea and selenodicysteine were recorded and compared with the XPS data obtained from the respective sulphur containing compounds. The oxidation state of selenium could be monitored by the observed chemical shifts of the Se(3p1/2),Se(3p3/2) and Se(3d3/2,5/2) levels. Though having a formal oxidation state near zero, the binding energy of the core electrons of Se in Se-methionine, Se-cystine and selenodicysteine was shifted by 0.4, 0.7 and 0.4 eV, respectively. This phenomenon was attributed to the rather distinct polarization of Se. The reversible oxidation of Se-cystine using H2O2 and NaBH4 could be successfully demonstrated by this XPS-technique.

Amino Acids↗
PubMed1975

Modification of a selenium toxicity in chicks by dietary silver and copper.

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.

Administration, Oral↗
PubMed1986

The metabolism of selenomethionine, Se-methylselenocysteine, their selenonium derivatives, and trimethylselenonium in the rat.

The formation of dimethylselenide (respiratory) and trimethylselenonium (urinary) metabolites from [75Se]selenomethionine, [75Se]methylselenomethionineselenonium, [75Se]methylselenocysteine, [75Se]dimethylselenocysteineselenonium, and [75Se]trimethylselenonium was determined using single sc doses of 2 or 0.064 mg Se/kg in male and female rats. The 75Se content of liver, kidney, pancreas, testis, spleen, blood, heart, brain, and skeletal muscle was determined at 0.5 and 24 h. Respiratory 75Se after 24 h was greatest from Se-dimethylselenocysteineselenonium (38 and 17% for the high and low doses, respectively). Respiratory 75Se was about 8% for the high dose of Se-methylselenocysteine and was less for all other compounds. Total 75Se excretion in the urine was highest from rats given trimethylselenonium (about 90%, both doses) and was lowest from rats given selenomethionine (4%, low dose). Urine samples were chromatographed on SP-Sephadex cation-exchange columns and 75Se was eluted with ammonium formate; trimethylselenonium was precipitated with ammonium Reineckete solution and trimethylsulfonium carrier. Urinary trimethylselenonium excretion was greatest from rats given trimethylselenonium, but rats given Se-dimethylselenocysteineselenonium (low dose) excreted 35-45% of the dose as trimethylselenonium ion. The lowest quantity of trimethylselenonium was excreted by rats given the low dose of selenomethionine (0-3%). Pancreas, kidney, and liver showed the highest uptake (% of dose/g) of the selenium compounds. Trimethylselenonium was highly concentrated by the kidney and also showed high myocardial uptake (heart/blood ratio = 5) 0.5 h after injection; the selective uptake of trimethylselenonium in heart was not observed for the other selenonium compounds.

Animals↗
PubMed1990

Subcellular distribution of selenoproteins in the liver of the rat.

After in vivo labeling with [75Se]selenite, the intracellular distribution of selenoproteins in the liver was investigated in selenium-adequate and selenium-deficient rats. In the subcellular fractions, which were obtained by differential centrifugation, the proteins were separated by means of SDS-PAGE and the selenium compounds were identified via their 75Se activity. In this way twelve selenium-containing proteins or protein subunits with molecular weights between 12,100 and 75,400 were found. Glutathione peroxidase was concentrated in the cytosol and in the mitochondria. With the newly detected selenoproteins, some were enriched in the cytosol, one was mainly found in the nuclear fraction and some, which were present mainly in the mitochondrial and microsomal fractions, are most probably membrane-bound. In the liver of selenium-depleted rats the selenium administered was used predominantly to restore the levels of some of the newly found selenoproteins, while in the liver of selenium-adequate animals most of the selenium retained was incorporated into the glutathione peroxidase. The differences in the distribution among the subcellular fractions and the specific incorporation of the element in selenium deficiency into certain compounds suggest that there are several metabolic pathways for selenium and that the selenoproteins are involved in several different processes of intracellular metabolism.

Animals↗