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At least 19 recordsLinked to original sources

Renal excretion of tellurium after peroral administration of tellurium in different forms to healthy human volunteers.

As tellurium ranks among the rare non-essential trace elements there is only little known of its intestinal absorption and its metabolic behaviour in humans. Data for risk evaluations needed for occupational medicine are based on animal experiments only. In order to investigate the metabolic behaviour of tellurium in man, tellurium in different forms was administered perorally to healthy male human volunteers. It was given as sodium tellurate, sodium tellurite, metallic colloid and intrinsically bound in cress. For the latter, cress was cultivated with tellurium-containing water in order to provide tellurium for ingestion in a form which is more equivalent to foodstuffs. After the administration the urinary excretion of tellurium was determined. Tellurium concentrations were measured in urine samples by means of graphite furnace atomic absorption spectroscopy (GFAAS) after wet ashing and a preconcentration of tellurium by solvent extraction with isobutyl methyl ketone (IBMK). From the cumulative tellurium excretion in the first four days after the administration, a percentage intestinal absorption of 25% +/- 10% for soluble tellurium salts can be calculated. The renal tellurium excretion is faster after administration of hexavalent tellurium than after ingestion of the tetravalent form. This can explain the higher toxicity of the tetravalent tellurium compounds found in animal experiments. The introduction of tellurium to cress lowered the intestinal absorption to approximately 15%. For metallic tellurium the fractional intestinal absorption was found to be about 10%.

Adult↗

Tribromo(3,5-dimethyl-2-nitrophenyl-kappa(2)C(1),O)tellurium(IV), bromo(3,5-dimethyl-2-nitrophenyl-kappa(2)C(1),O)tellurium(II) and bromo(3,5-dimethyl-2-nitrosophenyl-kappa(2)C(1),O)tellurium(II).

All three title compounds, prepared from bis(3,5-dimethyl-2-nitrophenyl)ditellurium, exhibit high degrees of intramolecular Te-O coordination. Their Te-O distances increase in the order C(8)H(8)BrNOTe < C(8)H(8)BrNO(2)Te < C(8)H(8)Br(3)NO(2)Te, with distances of 2.165 (3), 2.306 (1) and 2.423 (6) A, respectively, indicating that C(8)H(8)BrNOTe may be more aptly described as 1-bromo-4,6-dimethyl-2,1,3-benzoxatellurazole.

Journal Article↗

Incorporation of tellurium into amino acids and proteins in a tellurium-tolerant fungi.

Aspergillus fumigatus, Aspergillus terreus, and Penicillium chrysogenum, a tellurium tolerant fungi, are able to grow on sulfur free medium amended with 0.2% (w/v) tellurite. Tellurium was incorporated into several types of low and high molecular weight proteins. The newly detected telluro-proteins contained an extraordinary high level of tellurium, as well as telluro-cysteine, telluro-cystine, telluro-methionine, and serine.

Amino Acids↗

Large scale synthesis of tellurium nanoribbons in tetraethylene pentamine aqueous solution and the stability of tellurium nanoribbons in ethanol and water.

Superlong single crystal tellurium nanoribbons with a width of 200-300 nm and length up to several hundred micrometers have been synthesized in tetraethylene pentamine aqueous solution at 80 degrees C. The stability of as prepared tellurium nanoribbons in solvents such as pure ethanol and deionized water has been studied. The poor crystallinity of the initial single crystalline Te nanoribbons with prolonged storing time demonstrated that the initial single crystalline nanobelts tend to be destroyed and to dissolve in the solvent. In meantime, the supersaturation of the solvable Te species in such solvents will result in the formation of amorphous Te, and the formation of amorphous TeO2 due to partial oxidation of the Te nanostructures and the newly formed amorphous Te. The detailed corrosion process, crystallinity, and shape evolution process have been carefully examined by the XRD, TEM, HRTEM, and XPS techniques. This erosion phenomenon attacked by solvents has been not identified previously, suggesting that tellurium nanoribbons synthesized by other chemical methods could be also not stable in solution system and their storage after laboratory synthesis requires special attention.

Journal Article↗

Tellurium and tellurium dioxide: single endotracheal injection to rats.

Single endotracheal injections of tellurium and tellurium dioxide, at dosage levels sufficient to cause observable stress in rats, did not result in a progressive fibrotic tissue response after 180 days. The observation period of 180 days is insufficient to assess the lack of tumorigenic potential of these compounds and, therefore, no conclusions on this point are to be inferred.

Animals↗

trans-Tetrachlorobis(N, N'-dimethylimidazolidine-2-thione)tellurium(IV), a thiourea complex of tellurium with asymmetric Te-S bonds

The structure of the title compound, [TeCl(4)(C(5)H(10)N(2)S)(2)] or C(10)H(20)Cl(4)N(4)S(2)Te, has been solved in order to study the stereochemical activity of the lone pair of electrons on Te(IV). The two crystallographically independent molecules in the asymmetric unit both show a distorted octahedral coordination of the Te atom. The two Te-S bonds are trans to each other in both molecules and are greatly asymmetric, with bond lengths of 2.5686 (7) versus 2.8557 (8) A and 2.5859 (7) versus 2.8165 (9) A. The Te-Cl bond lengths lie in the range 2.5236 (7)-2.5589 (8) A. The asymmetric Te-S bonds and a large S-Te-Cl angle of ca 97 degrees involving the long Te-S bonds indicate stereochemical activity of the lone pair of electrons on Te.

Journal Article↗

Chlorotris(N,N'-dicyclohexylthiourea-S)tellurium(II) chloride, a tellurium complex with a TeClS3 coordination sphere.

During the synthesis of a series of square-planar [TeCl2(stu)2] complexes, where stu represents bulky di- or tetrasubstituted thioureas, the title compound, [TeCl[(C6H11NH)2CS]3]Cl or C39H72ClN6S3Te+*Cl-, was the unexpected result when stu was N,N'-dicyclohexylthiourea. The complex is square planar, with Te-S distances of 2.5803 (4), 2.6211 (4) and 2.8214 (4) A, and a Te-Cl distance of 2.6485 (4) A, indicating a small trans influence of the thiourea ligand.

Journal Article↗

Redox chemistry of tellurium bis(tert-butylamido)cyclodiphosph(V)azane disulfide and diselenide systems: a spectroscopic and structural study.

The redox chemistry of tellurium-chalcogenide systems is examined via reactions of tellurium(IV) tetrachloride with Li[(t)()BuN(E)P(mu-N(t)Bu)(2)P(E)N(H)(t)Bu] (3a, E = S; 3b, E = Se). Reaction of TeCl(4) with 2 equiv of 3a in THF generates the tellurium(IV) species TeCl(3)[HcddS(2)][H(2)cddS(2)] 4a [cddS(2) = (t)BuN(S)P(mu-N(t)Bu)(2)P(S)N(t)Bu] at short reaction times, while reduction to the tellurium(II) complex TeCl(2)[H(2)cddS(2)](2) 5a is observed at longer reaction times. The analogous reaction of TeCl(4) and 3b yields only the tellurium(II) complex TeCl(2)[H(2)cddSe(2)](2) 5b. The use of 4 equiv of 3a or 3b produces Te[HcddE(2)](2) (6a (E = S) or 6b (E = Se)). NMR and EPR studies of the 5:1 reaction of 3a and TeCl(4) in THF or C(6)D(6) indicate that the formation of the Te(II) complex 6a via decomposition of a Te(IV) precursor occurs via a radical process to generate H(2)cddS(2). Abstraction of hydrogen from THF solvent is proposed to account for the formation of 2a. These results are discussed in the context of known tellurium-sulfur and tellurium-nitrogen redox systems. The X-ray crystal structures of 4a.[C(7)H(8)](0.5), 5a, 5b, 6a.[C(6)H(14)](0.5), and 6b.[C(6)H(14)](0.5) have been determined. The cyclodiphosph(V)azane dichalcogenide ligand chelates the tellurium center in an E,N (E = S, Se) manner in 4a.[C(7)H(8)](0.5), 6a.[C(6)H(14)](0.5), and 6b.[C(6)H(14)](0.5) with long Te-N bond distances in each case. Further, a neutral H(2)cddS(2) ligand weakly coordinates the tellurium center in 4a small middle dot[C(7)H(8)](0.5) via a single chalcogen atom. A similar monodentate interaction of two neutral ligands with a TeCl(2) unit is observed in the case of 5a and 5b, giving a trans square planar arrangement at tellurium.

Journal Article↗

Lipid droplets in Schwann cells during tellurium neuropathy are derived from newly synthesized lipid.

Exposure of weanling rats to a diet containing elemental tellurium results in a peripheral neuropathy characterized by segmental demyelination and minimal axonal degeneration. One of the earliest ultrastructural abnormalities in tellurium neuropathy is an increased number of cytoplasmic lipid droplets in myelinating Schwann cells. The pathogenesis of these lipid droplets was investigated using light and electron microscopic autoradiography. Nerve lipids were either "prelabeled" with [3H]acetate via in vivo intraneural injection 3 days before a 2-day exposure to tellurium, or "postlabeled" via in vivo intraneural injection or in vitro incubation with [3H]acetate following a 2-day exposure to tellurium. In the prelabeled nerves, myelin became heavily labeled, but the tellurium-induced cytoplasmic lipid droplets were rarely labeled. In the postlabeled nerves, the tellurium-induced cytoplasmic lipid droplets were the most heavily labeled structures within the nerve. These data indicate that the tellurium-induced lipid droplets in Schwann cells are derived from newly synthesized lipid rather than from the early breakdown and internalization of myelin lipids. The earliest biochemical abnormality observed in tellurium neuropathy is an inhibition of cholesterol synthesis at the squalene epoxidase step. This leads to an accumulation of squalene within the nerve. We conclude that the cytoplasmic lipid droplets in Schwann cells contain this accumulated lipid.

Animals↗

Inhibition of human squalene monooxygenase by tellurium compounds: evidence of interaction with vicinal sulfhydryls.

Squalene monooxygenase is a flavin adenine dinucleotide-containing, microsomal enzyme that catalyzes the second step in the committed pathway for cholesterol biosynthesis. Feeding weanling rats a diet containing 1% elemental tellurium causes a transient, peripheral demyelination due to the disruption of cholesterol synthesis in Schwann cells secondary to inhibition of squalene monooxygenase. The tellurium species responsible for the inhibition is unknown, as is the mechanism of inhibition. To study the potential mechanisms of tellurium toxicity in humans, three likely in vivo metabolites of tellurium (tellurite, dimethyltellurium dichloride, and dimethyltelluride) were tested as inhibitors of purified human squalene monooxygenase. All three inhibitors reacted with the enzyme slowly and the resulting interaction was not freely reversible. The 50% inhibitory concentration for the methyltellurium compounds (approximately 100 nM) after a 30-min preincubation was 100-fold lower than that of tellurite, indicating a role for hydrophobicity in the enzyme-inhibitor interaction. The ability of glutathione and 2,3-dimercaptopropanol to prevent and reverse the inhibition indicated that the tellurium compounds were reacting with sulfhydryls on squalene monooxygenase, and the ability of phenylarsine oxide, which reacts specifically with vicinal sulfhydryls, to inhibit the enzyme indicated that these sulfhydryls are located proximal to one another on the enzyme. These results suggest that the unusual sensitivity of squalene monooxygenase to tellurium compounds is due to the binding of these compounds to vicinal cysteines, and that methylation of tellurium in vivo may enhance the toxicity of tellurium for this enzyme.

Arsenicals↗

Temporal relationship of blood-nerve barrier breakdown to the metabolic and morphologic alterations of tellurium neuropathy.

The appearance of endoneurial edema early in the evolution of tellurium neuropathy raises the possibility that a breakdown of the blood-nerve barrier (BNB) plays a role in the pathogenesis of the tellurium-induced demyelination. To investigate this possibility, we correlated the temporal onset of breakdown of the BNB with inhibition of cholesterol synthesis and ultrastructural abnormalities in sciatic nerve of weanling Long-Evans rats fed a diet containing 1.1% elemental tellurium. Permeability of the BNB was assessed with [125I]-albumin and horseradish peroxidase (HRP); cholesterol synthesis was assessed by incubating segments of sciatic nerve in vitro with [1-14C]acetate. Cholesterol synthesis was severely inhibited and labeled squalene was accumulating in sciatic nerve at 12 hr of tellurium exposure. The permeability of the BNB progressively increased between 24 hr and 72 hr of tellurium exposure. Membrane-delimited vacuoles, lipid droplets and cytoplasmic excrescences appeared in myelinating Schwann cells at 24 hr; demyelinating axons appeared at 48 hr of tellurium exposure. These observations suggest that factors other than BNB breakdown and vasogenic endoneurial edema are responsible for the initial Schwann-cell injury in tellurium neuropathy. However, the early onset of BNB breakdown may have a synergistic role in the pathogenesis of tellurium-induced demyelination.

Animals↗

Speciation analysis of tellurium by solid-phase extraction in the presence of ammonium pyrrolidine dithiocarbamate and inductively coupled plasma mass spectrometry.

Under acidic conditions tellurium(IV) formed a complex with ammonium pyrrolidine dithiocarbamate (APDC). The tellurium(IV) complex was completely retained on a non-polar Isolute silica-based octadecyl (C(18)) sorbent-containing solid-phase extraction (SPE) cartridge, while the uncomplexed Te(VI) passed through the cartridge and remained as a free species in the solution. Only partial Te(IV) was retained on the SPE cartridge for samples without addition of APDC. On the basis of different retention behaviours of the complexed Te(IV) and uncomplexed Te(VI), a simple and highly sensitive method is proposed for the determination of total tellurium and Te(VI) by SPE separation and inductively coupled plasma mass spectrometry (ICP-MS) detection. The Te(IV) concentration was calculated as the difference between total tellurium and Te(VI) concentrations. The detection limit (3 sigma) is 3 ng L(-1) tellurium. Factors affecting the separation and detection of tellurium species were investigated. Coexisting ions did not show significant interferences with the Te(IV)-APDC complex retention and the subsequent ICP-MS detection of Te. The method has been successfully applied to the tellurium speciation analysis in waters with spiked recoveries for Te(IV) and Te(VI) of 86.0-108% and 87.1-97.4%, respectively.

Mass Spectrometry↗

Use of platinum as a modifier in the sensitive detection of tellurium in biological samples.

Estimation of tellurium in biological samples by flameless atomic absorption spectrophotometry is hindered by the high volatility of the metal. This necessitates the use of low ashing temperatures which are inadequate to thoroughly ash the samples and thereby reduce interference due to smoke during the atomization stage. The use of platinum as a chemical modifier to thermally stabilize tellurium has, therefore, been explored. Thermal stability of tellurium was dependent on the concentration of platinum; maximum enhancement in stability was achieved at a platinum concentration of 10 microgram/ml or greater, which allowed ashing temperatures to be increased from 400 to 1300 degrees C. A threefold increase in the sensitivity for tellurium determination was also obtained in the presence of platinum. The thermal stability and the sensitivity, however, were susceptible to the presence of organic, inorganic, and biological matrices. This procedure for the determination of tellurium, stabilized probably in the form of an amalgam with platinum, has been used successfully to estimate tissue levels of the metal following administration to mice of a novel tellurium-containing immunostimulant agent. Detection limits in urine, plasma, and tissues were about 50, 5, and 170 ng of tellurium per milliliter or gram, respectively.

Animals↗