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PubMed1995

Inhibition of aflatoxin B1-induced cell injury by selenium: an in vitro study.

Dietary selenium is an essential trace element in human nutrition. Selenium has been shown in animal studies to inhibit aflatoxin hepatocarcinogenesis. However, the cellular mechanism responsible for the inhibition has not been thoroughly studied. This study examines the effect of two selenium compounds, namely, sodium selenite and selenium-enriched yeast extract (SeY), on the cytotoxicity, DNA-binding and mutagenicity of aflatoxin B1 (AFB1) in cultured Chinese hamster ovary (CHO) cells. CHO cells, after treatment with 2 micrograms ml-1 selenite or 80 micrograms ml-1 SeY, exhibited increased resistance to AFB1-induced cell killing. At a concentration of 50 micrograms ml-1 AFB1, cell survival, measured by the clonogenicity assay, was increased by 21- and 10-fold in selenite- and SeY-treated cells, respectively. However, selenium treatment did not appear to affect AFB1-DNA binding. Similarly, no effect was observed on AFB1 mutagenicity, as determined by the hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene mutation assay. The results showed that selenium could effectively protect cells from AFB1 cytotoxicity in cultured cells but had no effect on AFB1-DNA adduct formation or mutagenesis. It is suggested that there are multiple pathways of AFB1 toxicity and that selenium can modulate AFB1-induced cell killing independent of its genotoxicity.

Aflatoxin B1↗

PubMed1990

Chromosome aberrations, sister-chromatid exchanges and cell-cycle kinetics in human peripheral blood lymphocytes exposed to organoselenium in vitro.

The ability of 2 synthetic organoselenium compounds, a dimer of p-methoxybenzeneselenol (DPMBS) and benzylselenocyanate (BSC), to induce sister-chromatid exchanges (SCE) and chromosome aberrations (CA) as well as to alter the progression of the cell through mitosis has been investigated in cultured human lymphocytes. Cultures treated with the highest concentration (2.27 x 10(-5) M) of the 2 compounds exhibited about a 3-fold increase in the level of SCE and about 2-3-fold increase in the incidence of CA. In addition, the 2 selenium compounds led to an inhibition of cell proliferation as was evidenced by the depression of the proliferation rate index (PRI).

Adult↗

PubMed1995

Studies on the distribution and characteristics of new mammalian selenium-containing proteins.

It has now been established that the essential effects of selenium in mammals are owing to the presence of several biologically active selenium compounds. Seleno-enzymes identified so far include several glutathione peroxidases and the type 1 iodothyronine de-iodinase. Some other selenoproteins have been sequenced and characterized. After in vivo labelling of rats with 75Se and protein separation using gel electrophoretic methods, more than 25 selenium-containing proteins or protein sub-units were detected. Some of the results of the investigations on these compounds are summarized and discussed here. By determining the pattern in a large number of tissues information on the distribution of the selenium-containing proteins was obtained. Their biological significance is not yet known but several findings indicate that some of these proteins may have important functions, especially in the brain and the endocrine and reproductive organs. More detailed information is already available on a 34 kDa-protein found in the testis and spermatozoa. Studies on the effects of dosage and chemical form of dietary selenium indicated that the tissue levels of the seleno-enzymes are homeostatically controlled and cannot be increased by additional supply. The increase in the tissue selenium observed with high selenium intake was found to be mainly caused by the non-specific incorporation of the element into a large number or proteins. The formation of most of the other selenium-containing proteins has priority over that of the cytosolic and plasma glutathione peroxidases. Thus the selenium requirement, which was calculated for optimum plasma glutathione peroxidase activity, also covers the amounts needed for normal levels of the other biologically important selenium compounds.

Animals↗

PubMed1987

The effects of humic acid on the chemical and biological properties of selenium in the environment.

To shed light on the causes of Kaschin-Beck disease, which can be prevented by supplementation of the diet with sodium selenite, the interactions between inorganic selenium compounds (selenite and selenate) and humic/fulvic acid were investigated. Selenate was found to be slowly reduced to selenite by humic acid in acidic solution. Selenite was adsorbed on manganese dioxide and iron(III) oxide from solution to a much greater degree than on kaolin, humic acid, Yongshu soil, or silicon dioxide. Feeding mice a diet supplemented with sodium selenite increased the selenium concentration in the kidney, liver, spleen, lung, heart and blood. A diet containing sodium selenite and fulvic acid caused the selenium concentrations in the organs, with the exception of the spleen, to be lower than observed with the selenite-only diet. Selenium and fulvic acid increase the activity of glutathione peroxidase. Sodium selenite and fulvic acid injected in combination into the abdominal cavity of mice and rats were less toxic than either substance alone. Selenite and fulvic acid applied separately enhanced the luminosity of photobacterium phosphoreum T-3 at low concentrations but depressed the luminosity at higher concentrations. Selenite and fulvic acid in combination caused a larger enhancement and a smaller depression of the luminosity than observed with either substance alone. The hypothesis is formulated that Kaschin-Beck disease is caused by selenium levels insufficient to prevent the toxic effects of the organic compounds present in the drinking water of the regions in which the disease is endemic.

Animals↗

PubMed1994

Antioxidant activity of some diarylselenides in biological systems.

The selenoorganic compounds di(4-aminophenyl)selenide (10) and 4-nitro-4'-amino-diphenylselenide (36) were shown to inhibit lipid peroxidation in ADP/Fe2+/ascorbate-treated microsomes and tert-butylhydroperoxide-treated hepatocytes with IC50s of 3 and 10 microM, and 14 and 10 microM, respectively. In the former system, these inhibition constants compare favourably with those of Ebselen and classical antioxidants such as butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA). In the cell system, these selenium compounds were equipotent with BHA but more potent than Ebselen and its analogues. The diamino compound (10) was also an effective inhibitor of lipid peroxidation initiated by diquat redox cycling in hepatocytes, again being equipotent with BHA but more potent than Ebselen and its analogues, which actually stimulated lipid peroxidation in this test system. Manipulation of the amino functions of (10) and (36) by alkylation or acylation altered the antioxidant capacity. Optimal activity in this series was achieved by N-ethylation or N-isobutylation of (10). This produced antioxidants having IC50s below 1 microM in the microsome system, 3-13 microM in the tert-butylhydroperoxide system, and being 100% effective in the diquat model at 50 microM. On the other hand, acylation or alkylation of the amino groups with long chain acyl or alkyl groups reduced the efficacy of the structures below that of the parent diamine. As with other antioxidant compounds, several of the chalcogenides were relatively selective inhibitors of monocyte 5'-lipoxygenase-dependent secretion of LTB4 as compared to their effect on cyclooxygenase-dependent secretion of PGE2 (for example compound 42 had IC50s of 0.6 microM and 10 microM, respectively). No correlation was observed between the redox-properties of the chalcogenides and their respective abilities to inhibit these enzymes.

Adenosine Diphosphate↗

PubMed1982

Serum selenium levels in liver diseases.

A possible pathogenetic role of selenium deficiency in alcoholic cirrhosis of the liver has previously been discussed. In the present study serum selenium was analyzed in 5 groups of liver diseases. The method used for selenium determination was electrothermal atomic absorption, after thermal stabilization of selenium compounds by addition of nickel nitrate. The selenium level of a reference group of healthy Norwegian adults (n = 40) was 1.53 +/- 0.25 mumol/l. The serum concentrations of selenium in patients suffering from alcoholic cirrhosis, chronic active hepatitis and chronic persistent hepatitis were lowered to 40-80 per cent of those of the reference group. In alcoholic cirrhosis and chronic active hepatitis the decreased serum selenium concentrations were significantly correlated to decreased levels of albumin and prealbumin.

Hepatitis, Chronic↗

PubMed1981

Metal interactions in carcinogenesis: enhancement, inhibition.

Metals constitute a fundamentally important part of the total human environment. Since human exposure often involves complex mixtures of metal compounds and, possibly, organic compounds which may be carcinogenic per se, interactions between these compounds may add significantly to human cancer risk. Our present knowledge about these kinds of interactions is very limited. The best investigated area is benzo(a)pyrene (BP)-metal oxide particle interactions in respiratory carcinogenesis in the hamster. Metal oxide particles were also shown to modify the carcinogenic effect of nitrosamines. Several reports describe experiments in which selenium compounds exerted a generally anticarcinogenic and antimutagenic activity. Inorganic arsenic compounds, which are accepted to be carcinogenic in man, have so far been negative in animal experiments except for one recent suggested report. Several authors have, however, suggested that these compounds may act as cocarcinogens due to their inhibition of DNA repair, although animal experiments to demonstrate a cocarcinogenic effect of arsenic compounds have been negative so far, except for one preliminary report. The concentration of zinc in the diet seemed to influence both transplanted tumor growth and the carcinogenicity of several organic compounds, and the possibility of a correlation between dietary zinc and certain cancer forms in man has been suggested. Protection against development of Leydigiomas usually induced by cadmium injection was afforded by simultaneous injection of zinc salts. Nickel carcinogenesis has been reported to be antagonized by manganese, and synergism between Ni and organic carcinogens, e.g. BP, has been demonstrated. There is no firm evidence that lead may be a cocarcinogen, although some limited experimental evidence is available. Oxidizing agents have been demonstrated to increase, and reducing agents to antagonize, the mutagenic effect of chromium compounds in vitro. The content of carcinogenic and other metals in asbestos has been suggested to modify the carcinogenic properties of asbestos. Since much of the information available at present is suggestive, further research on these interactions as well as other possible interactions in metal carcinogenesis is needed. Studies should be made both in well defined in vitro systems and in relevant animal models.

Animals↗

PubMed1989

Mercury-selenium interaction: distribution and excretion of 203Hg2+ in rats after simultaneous administration of selenite or selenate.

In female rats intravenously injected with 203HgCl2 (0.6 mg Hg2+ per kg body wt.) the effect of intraperitoneal administration of selenite or selenate (0.525 mg Se per kg body wt.) on distribution and excretion of 203Hg was studied. The content of 203Hg was lower in kidney and higher in liver and blood in the groups treated with selenate or selenite when compared with rats which received only mercury. The brain content of 203Hg was significantly increased in rats injected with selenite. Both selenium compounds injected immediately after mercury significantly decreased urinary as well as biliary excretion of 203Hg. A transient increase in the rate of biliary excretion of 203Hg during the first 2 h after administration was observed in rats treated with selenate. This finding seems to support the idea that the reduction of selenate to selenite in the body is not rapid but takes at least several hours.

Animals↗

PubMed1986

A novel biologically active seleno-organic compound--VI. Protection by ebselen (PZ 51) against galactosamine/endotoxin-induced hepatitis in mice.

Male albino NMRI mice were given 700 mg/kg galactosamine and 33 micrograms/kg salmonella endotoxin intraperitoneally. After 9 hr, serum sorbitol dehydrogenase activity had risen from 60 to 7320 U/l, SGOT from 90 to 5580, and SGPT from 70 to 10,440. When a similar dose of galactosamine alone or endotoxin alone was given, no significant liver injury was found. Animals pre-treated with an oral dose of ebselen (600 mg/kg 1-3 hr before galactosamine/endotoxin administration) were fully protected against this type of hepatitis. When pretreated 1 hr before intoxication with different doses of ebselen, significant dose-dependent reduction of serum enzyme activities was observed at doses higher than 1 mg/kg. After pre-treatment with 6 mg/kg ebselen, no biochemical or histological signs of liver lesions were detectable 36 hr after intoxication. In order to comparatively evaluate the model used, several established anti-inflammatory drugs were administered at doses which showed 50% effectiveness in preventing carageenan paw edema. A dose of 200 micrograms/kg dexamethasone, or 9 mg/kg indomethacin abolished galactosamine/endotoxin-induced enzyme release in our animals, as did the lipoxygenase pathway inhibitor diethylcarbamazine (78 mg/kg). In contrast, administration of cyclooxygenase pathway inhibitors such as aspirin (220 mg/kg) or ibuprofen (45 mg/kg) failed to prevent hepatitis. The effect of ebselen was also investigated in four different models of acute drug-induced liver damage. A dose of 600 mg/kg of the organic selenium compound was ineffective or weakly active in benzo(alpha)pyrene- or phenobarbital-treated mice which were intoxicated by intraperitoneal administration of 350 or 400 mg/kg body weight of paracetamol. Similarly negative results were obtained against bromobenzene-induced hepatotoxicity (520 mg/kg bromobenzene i.p.), carbon tetrachloride intoxication (3.2 g/kg), or allyl alcohol-induced liver damage (60 mg/kg). The selective efficacy of ebselen against galactosamine/endotoxin induced liver damage is interpreted in terms of its recently recognized ability to inhibit the formation of leukotrienes.

Alanine Transaminase↗

PubMed1996

Selenite and selenate inhibit human lymphocyte growth via different mechanisms.

Selenium compounds like selenite and selenate have strong inhibitory effects, particularly on mammalian tumor cell growth by unknown mechanisms. We found that the addition of sodium selenite and sodium selenate inhibited the growth of human 3B6 and BL41 lymphocytes. Selenite was more potent because 10 microM selenite produced a growth inhibitory effect similar to that of 250 microM selenate. The mechanism of action of selenite and selenate appears to be different. 3B6 and BL41 cells treated with selenite accumulated in the S-phase; however, selenate caused an accumulation of cells in G2. Selenite-mediated growth inhibition was irreversible, although the effects of selenate could be reversed. Selenite, in contrast to selenate, is efficiently reduced by the thioredoxin system (thioredoxin, thioredoxin reductase, and NADPH). At concentrations required to observe a similar effect on cell growth, the activity of thioredoxin reductase, recently shown to be a selenoprotein, increased in selenite-treated cells and decreased in selenate-treated cells. Ribonucleotide reductase activity was inhibited in an in vitro assay by selenite and selenodiglutathione but not by selenate. These results show that selenite and selenate use different mechanisms to inhibit cell growth.

B-Lymphocytes↗

PubMed1985

Selenium absorption by canine jejunum.

Deficiency of the trace element selenium causes disease in domestic animals and may also be implicated in the pathogenesis of some human illness. In this study, the triple-lumen perfusion method was used to measure the rate of absorption of trace quantities of selenium (50 micrograms/liter in a physiological electrolyte solution) from the jejunum when given as D,L-selenomethione, D,L-selenocystine, or sodium selenite to healthy dogs in vivo. Selenium absorption from the test segment (expressed as percent administered dose per centimeter +/- SEM) was 1.97 +/- 0.04 from D,L-selenomethionine, 1.15 +/- 0.06 from D,L-selenocystine, and 0.51 +/- 0.07 from sodium selenite (P less than 0.01, N = 5). In separate studies in four anesthetized dogs, the jejunum was perfused with L-[75Se] selenomethionine while concentrations of 75Se were measured in the portal venous blood; these studies established that [75Se]selenomethionine disappearing from the gut lumen corresponded quantitatively to 75Se appearing in the portal venous effluent (74 +/- 6%) and incorporated into intestinal tissue (24 +/- 5%). These results are consistent with the hypothesis that the absorption of amino acid-bound selenium is accelerated by the specific amino acid active transport mechanisms in the gut mucosa. Sodium selenite is absorbed more slowly, possibly by simple diffusion through the intestinal mucosa, than the amino acid-bound selenium compounds.

Animals↗

PubMed1994

Comparative effect of inorganic and organic selenocyanate derivatives in mammary cancer chemoprevention.

Recently El-Bayoumy and coworkers have reported that 1,4-phenylene-bis(methylene)selenocyanate (p-XSC) was very effective in inhibiting 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis and adduct formation during the initiation phase (Cancer Res., 52, 2402-2407, 1992). Furthermore, this compound was found to be well tolerated by rats at high doses. The present study was designed to extend these earlier observations by investigating the response to lower levels of p-XSC given either before or after DMBA administration. At a level of 15 p.p.m. Se, p-XSC suppressed total mammary tumor yield by 80% and 52% in the initiation phase and post-initiation phase, respectively. A dose-response effect was evident in the range 5-15 p.p.m. Se. When p-XSC was given at a level of 5 p.p.m. Se during the entire course of the experimental period, total tumor yield was reduced by half. This dose is about 4 x less than the maximum tolerable dose (MTD). Other selenocyanate analogs were also examined in an attempt to obtain information on their respective chemopreventive index, which is calculated as the ratio of MTD to the effective dose which produces approximately a 50% inhibition in total tumor yield (ED50). The reagents studied included potassium selenocyanate, methyl selenocyanate and benzyl selenocyanate, as well as sodium selenite (reference compound). Compared to p-XSC, which has a chemopreventive index of 4.0, the other four compounds have a lower index ranging from 1.3 for sodium selenite and potassium selenocyanate to 2.0 for methyl selenocyanate and 2.5 for benzyl selenocyanate. A high chemopreventive index signifies that a compound is well tolerated at doses required for cancer suppression. The last component of the present study involved the repletion assay of liver glutathione peroxidase in selenium-deficient rats as a biomarker to estimate the metabolizability of the above selenium compounds. The bioavailability data suggest that the selenium from p-XSC is not as efficiently incorporated into glutathione peroxidase as the selenium from selenite or the other selenocyanate analogs. Currently, we are working under the hypothesis that the chemical structure of the RSeCN compound could affect activity per se and also influence the rate of release of selenium from the parent compound, thereby impacting on the anticarcinogenic efficacy, tolerance and bioavailability of the compound.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1994

Selenium and the selenium-dependent glutathione peroxidase in rheumatoid arthritis.

Selenium is an essential component in the two antioxidant enzymes glutathione peroxidase (GSH-Px) and phospholipid hydroperoxide glutathione peroxidase (PLGSH-Px). Free oxygen radicals are involved in the inflammatory process seen in rheumatoid arthritis (RA) and are generated mainly through the phagocytic activity of the polymorphonuclear leucocytes. Several experimental studies indicate that selenium is important to the functioning of the immune system and to the inflammatory process. A low selenium status among patients with RA has been reported from areas with both high and low natural selenium intake. The reduction in the serum level is approx. 10%. This reduction is related to the clinical disease activity in arthritis patients in both cross-sectional and longitudinal studies, and selenium concentrations have been found to fluctuate during the disease. Reduced selenium concentrations have been reported in red blood cells, too, and concentrations have been found to be slightly reduced in the polymorphonuclear leucocytes. Studies do not agree on the activity of GSH-Px among RA patients. Thus activity levels have been reported to range from low to high. Those studies that have focused on the subgroup of patients with high persistent disease activity have reported reduced GSH-Px activities in both serum, red blood cells and polymorphonuclear leucocytes. Selenium supplementation using organic selenium compounds in doses of around 250 microgram/day increases the selenium concentration in serum and red blood cells considerably. However, supplementation is not reflected in the selenium level in polymorphonuclear leucocytes from RA patients as opposed to healthy subjects, in whom the level of selenium in polymorphonuclear leucocytes increases. Selenium supplementation increased GSH-Px activity in serum, red blood cells and platelets from RA patients, but in the polymorphonuclear leucocytes the increase was not sufficient to reach the levels of the controls. This apparent lack of de novo synthesis of GSH-Px in polymorphonuclear leucocytes from RA patients may be explained by their inability to increase their selenium content in spite of high levels of available extracellular selenium. this may be in accordance with the lack of anti-arthritic effect of selenium supplementation in controlled clinical studies among RA patients. Several experimental studies have reported inhibition of GSH-Px by antirheumatic drugs, in particular gold. In addition, gold has been found to reduce selenium in rat plasma. These interactions can, however, be modified by increasing the amount of selenium in the feed. Among RA patients there is no clear evidence of an interaction between gold, selenium and GSH-Px.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMedDate not supplied

Role of glutathione in selenite binding by human plasma.

The erythrocyte-mediated reduction of selenite has been reproduced by the addition of reduced glutathione to plasma at levels comparable to those present in the erythrocyte. The reaction has been followed by chromatography and ultraviolet (UV) absorption spectroscopy (in the absence of plasma). The first detectable compound, selenium diglutathione, is very unstable in physiological conditions. The product of the reaction does not contain glutathione and is able to react and incorporate selenium into plasma proteins without the participation of hemoglobin or glutathione reductase. A saturable low molecular weight compound is also able to bind selenium, which may be relevant in the initial distribution and excretion of selenium after selenite administration.

Blood Proteins↗

PubMed1977

Metals as mutagens.

A number of metals are mutagenic in bacteria or phage. These include compounds of arsenic, chromium, copper, iron, manganese, molybdenum, platinum, and selenium. Compounds containing alumium, antimony, arsenic, cadmium, copper, lead, mercury, nickel, and tellium have been shown to induce chromosomal aberrations or abnormal cell divisions in animal or plant cells. Genetic evidence suggests that arsenic, chromium, and molybdenum compounds may influence the accuracy of DNA repair processes in microorganisms.

Animals↗

PubMed1996

The inhibition of radiation-induced mutagenesis by the combined effects of selenium and the aminothiol WR-1065.

In order to evaluate the anti-mutagenic effects of the potential chemoprotective compounds selenium and (S)-2-(3-aminopropylamino)ethylphosphorothioic acid (WR-1065), CHO AA8 cells were exposed to both compounds either individually or in combination prior to irradiation. Mutation frequency following exposure to 8 Gy was evaluated by quantitation of the mutations detected at the hprt locus of these cells. Protection against radiation-induced mutation was observed for both 30 nM sodium selenite or 4 mM WR-1065. In addition, the protection against mutation induction provided by the combination of these agents appeared additive. In contrast, sodium selenite did not provide protection against radiation toxicity when provided either alone or in conjunction with WR-1065. In order to evaluate the possible mechanisms of the anti-mutagenic effects observed in these cells, glutathione peroxidase (GPx) activity was evaluated following exposure to the chemopreventative compounds. The addition of sodium selenite to the culture media resulted in a 5-fold increase in GPx activity, which was unaltered by the presence of the WR-1065. Northern analysis of RNA derived from these cells indicated that selenium supplementation resulted in a marginal increase in the mRNA for the cytosolic GPx (GSHPx-1) which was insufficient to account for the stimulation of GPx activity observed in cellular extracts. These results suggest that selenium and WR-1065 offer protection via independent mechanisms and that GPx stimulation remains a possible mechanism of the anti-mutagenic effect of selenium.

Animals↗

PubMed1972

Dimethylselenide and dimethyltelluride formation by a strain of Penicillium.

A strain of Penicillium which produced dimethylselenide from inorganic selenium compounds was isolated from raw sewage. Sulfate and methionine enhanced growth of the fungus and its production of dimethylselenide in media containing selenite. In solutions containing selenate, methionine inhibited dimethylselenide formation while stimulating proliferation of the fungus. Dimethylselenide was also generated from inorganic selenide. Alkylation did not appear to be a significant mechanism of selenium detoxication by this organism. Dimethyltelluride was also produced by the organism from several tellurium compounds, but this product was synthesized only in the presence of both tellurium and selenium. The yields of dimethylselenide and dimethyltelluride varied with the relative concentrations of selenium and tellurium in the medium.

Alkylation↗

PubMed1987

Periodate-oxidized adenosine inhibits the formation of dimethylselenide and trimethylselenonium ion in mice treated with selenite.

The metabolic detoxification of selenite and many other selenium compounds involves a series of S-adenosylmethionine-dependent methylations yielding dimethylselenide (DMSe), which is exhaled, and trimethylselenonium ion (TMSe), which is excreted in the urine. This paper shows that periodate-oxidized adenosine (Adox) inhibits these methylation reactions in vivo and increases the toxicity of selenite. When Adox was injected in mice at 100 mumol/kg 30 min before injection of [75Se]selenite at 0.4 mg Se/kg the appearances of [75Se]DMSe in the breath and [75Se]TMSe in the liver were completely inhibited for 90 min. This was mediated by accumulation of S-adenosylhomocysteine, the methyltransferase inhibitor, in the livers of Adox-treated mice due to inhibition of its hydrolase enzyme. During 24 h, Adox-treated mice excreted no detectable urinary [75Se]TMSe and exhaled only 20% as much [75Se]DMSe as controls. The urine of Adox-treated mice also contained S-adenosylhomocysteine at a level (ca. 4 mM), 200 times that of untreated mice, which provided a convenient index of methylation potential in the intact animal. When three groups of three mice each were injected with 100 mumol Adox/kg, selenite at 4 mg Se/kg, or a combination of the two, the mice receiving the combination were dead within 2 days, while the mice in the other two groups all survived at least 4 days. These results verify the enzymatic nature of selenium methylation in vivo, support its importance in detoxification, and indicate the value of Adox in further studies of selenium metabolism.

Adenosine↗