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PubMed1989

Selenium-containing tRNA(Glu) and tRNA(Lys) from Escherichia coli: purification, codon specificity and translational activity.

In response to low (approximately 1 microM) levels of selenium, Escherichia coli synthesizes tRNA(Glu) and tRNA(Lys) species that contain 5-methylaminomethyl-2-selenouridine (mnm5Se2U) instead of 5-methylaminomethyl-2-thiouridine (mnm5S2U). Purified glutamate- and lysine-accepting tRNAs containing either mnm5Se2U (tRNA(SeGlu), tRNA(SeLys] or mnm5S2U (tRNA(SGlu), tRNA(SLys] were prepared by RPC-5 reversed-phase chromatography, affinity chromatography using anti-AMP antibodies and DEAE-5PW ion-exchange HPLC. Since mnm5Se2U, like mnm5S2U, appears to occupy the wobble position of the anticodon, the recognition of glutamate codons (GAA and GAG) and lysine codons (AAA and AAG) was studied. While tRNA(SGlu) greatly preferred GAA over GAG, tRNA(SeGlu) showed less preference. Similarly, tRNA(SGlu) preferred AAA over AAG, while tRNA(SeLys) did not. In a wheat germ extract--rabbit globin mRNA translation system, incorporation of lysine and glutamate into protein was generally greater when added as aminoacylated tRNA(Se) than as aminoacylated tRNA(S). In globin mRNA the glutamate and lysine codons GAG and AAG are more numerous than GAA and AAA, thus a more efficient translation of globin message with tRNA(Se) might be expected because of facilitated recognition of codons ending in G.

Cell-Free System↗
PubMed1999

An acute intratracheal selenium study: immediate effects on respiration in guinea pigs.

Pulmonary function was assessed in non-sensitized male guinea pigs (206-445 g) before and after intratracheal (ITr) treatment with saline or selenium (Se, 0.06 mg/100 g body weight) as selenium dioxide (SeO2) or seleno-L-methionine (SeM). Pulmonary functional parameters such as the respiratory rate (f), tidal volume (TV), dynamic lung compliance (Cdynl) and lung resistance (Rl) were determined using the respiratory flow (F) signal and the transpulmonary signal obtained via the intrapleural pressure (P) from the animal. Although, pulmonary dysfunction was observable with exposure to two different Se compounds, the SeO2-induced changes in f and Rl were significant (P < 0.05). Treatment with SeM did not result in alteration of any of the parameters significantly. Results indicated that acute ITr SeO2 exposure affects respiration precipitated by a significantly decreased f and an increased Rl unlike after SeM. The Cdynl did not change significantly after treatment with either of the two Se compounds. Comparing the immediate effects of the two different Se compounds on respiration, acute ITr SeO2 exposure was found to be more detrimental to pulmonary function than SeM.

Animals↗
PubMed1978

Mercury metabolism in Japanese quail. I. The effect of dietary mercury and selenium on their tissue distribution.

Immature and adult coturnix quail were fed isolated soybean protein diets to which methylmercuric chloride or mercuric chloride were added with or without supplemental selenium for seven days. Samples of brain, blood, liver, and kidney were analyzed for total mercury and selenium via atomic absorption spectrophotometry. Selenium addition had no effect on the mercury concentration in kidney, brain, or blood but did tend to increase the concentration of mercury in the livers of the methylmercuric chloride-treated birds. Selenium in the presence of methylmercury increased the selenium concentration of liver and kidney but had little effect on the selenium concentration of brain or blood. Methylmercuric chloride supplementation resulted in increased selenium concentration in the blood of the selenium supplemented group. All other tissue selenium levels were unaffected by the addition of mercury.

Animals↗
PubMed1980

Selenium inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis in the rat.

The effect of supplemental dietary selenium on the postinitiation state of N-methyl-N-nitrosourea (MNU)-induced mammary carcinogenesis was investigated in noninbred female Sprague-Dawley rats. Mammary cancer was induced by a single iv injection of MNU. Supplemental selenium feeding was begun 7 days after carcinogen treatment. Feeding of selenium prolonged the latency of mammary cancer appearance and resulted in a reduction in the average number of cancers per rat. The results suggested an inhibitory effect of pharmacologic levels of dietary selenium on the postinitiation stage of mammary carcinogenesis.

Adenocarcinoma↗
PubMed1987

The two faces of selenium.

The nutritionally important trace elements share a high biological activity, implemented through association with enzymes, hormones or vitamins. The same activity responsible for physiological responses at extremely low dietary levels implies the potential for metabolic upset when the elements are ingested at elevated, although still relatively low levels. Selenium provides a classic example of this dichotomy of effects and has generated concerns at both ends of its supply spectrum. Experiences in the Dakotas, mid-19th century, led to identification of toxicity symptoms for which selenium was later shown to be responsible, while separate studies showed that excess selenium was teratogenic in the developing avian fetus. These toxic reactions suggested that selenium might be useful in restricting abnormal cell growth, and recent studies have proved it to be anticarcinogenic in certain specific circumstances. Investigation of selenium's nutrient function has been equally interesting, and when Schwarz showed it to be an essential nutrient in 1957, he began an era of intense research activity. Dietary levels of selenium below 0.02 ppm were found to cause deficiency symptoms affecting muscles, liver and pancreas and glutathione peroxidase was shown to be an active form through which selenium acted to prevent such aberrations. Research continues to seek other active organic combinations for selenium to identify interfering compounds that restrict its bioactivity and to explore biochemical mechanisms involved in its toxicity.

Aged↗
PubMed1989

Toxicity of selenium (Na2SeO3) and mercury (HgCl2) on the planarian Dugesia gonocephala.

The toxicity of selenium (Na2SeO3) and mercury (HgCl2) was determined by using a freshwater planarian which is particularly sensitive to pollution, and belongs to a fissiparous breed of Dugesia gonocephala. The mortality and fissiparity frequency of the subjects were studied. They were exposed to intense treatments (48 hours) or for medium to long periods of time (21 days) to either the single compounds or a combination of both, and were fed or fasting. The lethal effect of sodium selenite is correlated to the food intake, whereas the toxicity of mercurous chloride is probably the result of a fixative effect which does not depend on feeding. The 21-day treatment with the first compound has a non-negligible lethal effect which is probably due to an accumulation phenomenon. At doses where an antioxidant effect prevails, fissiparity is stimulated. On the other hand, the second compound reduces reproduction frequency to half the base values. Compared to the Paracentrotus lividus, the Dugesia gonocephala offers various advantages concerning toxicological experiments; besides being easier to handle in the laboratory, it is available all year round and is not subject to seasonal cycles. It is also more susceptible to the toxic effect of mercury, which is a common and highly toxic pollutant, than the sea urchin.

Animals↗
PubMed2006

Availability and metabolism of 77Se-methylseleninic acid compared simultaneously with those of three related selenocompounds.

Nutritional selenocompounds are considered to be transformed into the common intermediate selenide for utilization as selenoenzymes and/or for excretion as selenosugar and trimethylselenonium (TMSe). Therefore, selenocompounds can only be traced with a labeled selenium atom. Methylseleninic (MSA(IV)) has been proposed to be a third nutritional selenium source, the other two being inorganic selenocompounds and organic selenoamino acids, and to be a proximate selenochemical for producing the assumed biologically active form methylselenol. Here we applied a new tracer method to compare the availability and metabolism of MSA(IV) with those of three related selenocompounds under exactly identical host and tracing conditions. (82)Se-Selenite, (78)Se-selenate, (77)Se-MSA(IV) and (76)Se-methylselenonic acids (MSA(VI)) were simultaneously administered orally, each at the dose of 25 microg Se/kg body weight, to rats that had been depleted of endogenous natural abundance selenium with a single stable isotope ((80)Se). Time-related changes in the concentrations and/or distributions of the four labeled isotopes in the serum, liver, kidney, pancreas, lung and urine were determined simultaneously by inductively coupled argon plasma mass spectrometry (ICP MS) and/or HPLC-ICP MS. The availability with different isotope ratios was in the decreasing order of selenate>selenite=MSA(IV)>MSA(VI). Although selenate and MSA(VI) were distributed in organs and urine partly in their intact forms, MSA(IV) and selenite were not detected in the intact forms at all. MSA(IV) and MSA(VI) but not selenite or selenate produced TMSe in organs other than the liver, suggesting the transformation of MSA(IV) into methylselenol, and then either into selenide for the synthesis of selenoproteins and selenosugar or directly into TMSe. Thus, selenosugar and TMSe were produced widely in the organs. However, TMSe was not detected in the liver. The organ- and selenium source-specific production of TMSe was discussed as to the differences in selenium sources, and demethylation and methylation activity.

Administration, Oral↗
PubMed2006

Inhibition of DMBA induced rat mammary duct damage by novel synthetic organoselenium compounds.

The balance between prooxidants and antioxidants is crucial to the survival and functioning of aerobic organisms. Partially reduced derivatives of oxygen, which are produced in aerobic organisms as part of normal physiological and metabolic processes, are toxic species, oxidizing numerous biomolecules, which initiate tissue injury and cell death. DMBA (7,12-dimethylbenz[a]anthracene) is a polycyclic aromatic hydrocarbon (PAH) known to cause tumors in rats. DMBA is known to generate DNA-reactive species, which may enhance oxidative stress in cells, during its metabolism. Besides the formation of DNA adducts, oxidative products derived from mutagen metabolism, such as DMBA, might impair vital cellular functions by damaging proteins and lipid membranes. Synthetic organoselenium compounds inhibit the initiation phase of carcinogenesis by inhibiting DMBA-DNA adduct formation in the target organ in vivo. Because of the health problems induced by many environmental pollutants, many efforts have been undertaken to evaluate the relative antioxidant potential of selenium and synthetic organoselenium compounds. We undertook the present study to evaluate the chemopreventive potential of the novel synthetic organoselenium compounds (1-isopropyl-3-methylbenzimidazole-2-selenone (SeI) and 1,3-di-p-methoxybenzylpyrimidine-2-selenone (SeII)) in the well-established DMBA-treated rat model by monitoring the extent of lipid peroxidation and mammary duct damage. In this study, adult female Wistar rats were treated with DMBA and the novel organoselenium compounds (SeI and SeII) in determined doses. In DMBA-treated rats, the effects of the organoselenium compounds on malondialdehyde (MDA) levels and histological changes in the rat mammary lactiferous duct were studied. The ability of the organoselenium compounds to prevent oxidative damage induced by DMBA in rat mammary ducts was demonstrated. Protection against lipid peroxidation measured as MDA in the SeI and SeII treated groups was provided by the novel synthesized organoselenium compounds. SeI and SeII both provided chemoprevention against DMBA-induced oxidative stress in the rat mammary duct.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2006

Metabolic transformation of methylseleninic acid through key selenium intermediate selenide.

Methylseleninic acid (MSA(IV)) [CH(3)Se(O)OH] is readily reducible to methylselenol [CH(3)SeH], the assumed lyase metabolite and the proposed biologically active form of methylated selenoamino acids. At the same time, MSA(IV) is an oxidation product of the major urinary metabolite selenosugar. (77)Se-Enriched MSA(IV) was injected intravenously into rats (25 microg Se/kg body weight), and urine, blood and liver were obtained at five time points after the injection. Time-related changes in the concentration of (77)Se were determined together with speciation analysis of the labeled metabolites. (77)Se was mostly moved into red blood cells (RBCs) within 10 min, and then redistributed into organs within 30 min. Excessive (77)Se taken up by the liver was first detected as selenosugar A and then as B, suggesting that MSA(IV) was transformed to selenide, and then to selenosugar A followed by methylation to selenosugar B (urinary metabolite). (77)Se was incorporated also into selenoproteins (most efficiently to plasma selenoprotein P that is synthesized in liver), suggesting that MSA(IV) is utilized for the synthesis of selenosugar (for excretion) and selenoproteins (for utilization) through selenide. In vitro experiments with simultaneous incubation of (77)Se-MSA(IV) and (82)Se-selenite in a RBC suspension revealed the precise difference in the metabolism between MSA(IV) and selenite in RBCs. (77)Se excreted into the urine was mostly detected as selenosugar but with a distinct amount of trimethylselenonium, suggesting that selenosugar and trimethylselenonium are produced depending on the capacity to transform methylselenol to selenide. MSA(IV) was suggested to be reduced to methylselenol (allowing the production of a proposed active form of selenium), and then transformed (demethylated) to selenide for utilization and excretion.

Animals↗
PubMed2004

Oxidative stress in mothers who have conceived fetus with neural tube defects: the role of aminothiols and selenium.

BACKGROUND & AIMS: Methionine metabolic impairment and selenium deficit have been associated to neural tube defects. The relationship between thiol metabolism and selenium is not well known. We assessed the status of aminothiols and selenium, as well as thiolic status and the amino acids involved in arginine synthesis in the case of selenium depletion and repletion, studying their relationship to neural tube defects. METHODS: We studied 44 women of 37 +/- 8 years (mean +/- SD) who had conceived fetuses with neural tube defects as cases; and 181 women of 39 +/- 7 years (mean +/- SD) with healthy children as controls. We determined selenium, vitamin B12, serum folates, plasma thiol compounds and amino acids. Homocysteine transsulfuration was assessed using total cysteine/total homocysteine ratio (tCys/tHcy), and selenium repletion cut-off value was 1.06 micromol/l (84 microg/l). RESULTS: Cases showed significantly lower levels (median) than controls of total homocysteine (P = 0.001), total cysteinylglycine (P < 0.001), selenium (P < 0.001) and tryptophane (P = 0.002); and higher tCys/tHcy levels (P < 0.001), glutathione (P = 0.008) and L-arginine (P = 0.001). Cases with selenium depletion (selenium < or = 1.06 micromol/l) had significantly higher levels than controls of cysteine (P = 0.010), glutathione (P = 0.005), tCys/tHcy (P < 0.001), and arginine (P = 0.004), but significantly lower levels than controls of tryptophane (P = 0.027), cysteinylglycine (P < 0.001) and folates (P < 0.001). Only cysteinylglycine was lower than controls (P < 0.001) when selenium > 1.06 micromol/l. Methionine levels were higher in cases with selenium depletion than in repletion (P = 0.029). CONCLUSIONS: According to our data, a diet deficient in selenium and folates or their absorption impairment, and/or other mechanisms related to polyamines and nitric oxide can lead to oxidant/antioxidant imbalance and to a higher occurrence of these malformations.

Adult↗

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