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PubMed1997

Tellurium causes dose-dependent coordinate down-regulation of myelin gene expression.

Exposure of developing rats to a diet containing elemental tellurium systemically inhibits cholesterol synthesis at the level of squalene epoxidase. At high tellurium exposure levels (> 0.1% in the diet), there is an associated segmental demyelination of the PNS. Low levels of dietary tellurium (0.0001%) led to in vivo inhibition of squalene epoxidase activity in sciatic nerve, and inhibition increased with increasing exposure levels. With increasing dose and increasing exposure times, there was an increasing degree of demyelination and increasing down-regulation of mRNA levels for myelin P0 protein, ceramide galactosyltransferase (rate-limiting enzyme in cerebroside synthesis), and HMG-CoA reductase (rate-limiting enzyme in cholesterol synthesis). Because these were all down-regulated in parallel, we conclude there is coordinate regulation of the entire program for myelin synthesis in Schwann cells. An anomaly was that at early time points and low tellurium levels, mRNA levels for HMG-CoA reductase were slightly elevated, presumably in response to tellurium-induced sterol deficits. We suggest the eventual down-regulation relates to a separate mechanism by which Schwann cells regulate cholesterol synthesis, related to the need for coordinate synthesis of myelin components. Levels of mRNA for the low-affinity nerve growth factor receptor (indicator of alterations in axon-Schwann cell interactions) and for lysozyme (marker for phagocytic macrophages) were both up-regulated in a dose- and time-dependent manner which correlated with the presence of segmental demyelination. Levels of mRNA coding for myelin-related proteins were down-regulated at low tellurium exposure levels, without demyelination or up-regulation of nerve growth factor receptor. This suggests the down-regulation is related to the tellurium-induced cholesterol deficit, and not to the loss of axonal contact associated with early stages of demyelination or to the entry of activated macrophages.

Acetates↗
PubMed1991

Stable isotopes for determining biokinetic parameters of tellurium in rabbits.

We have compared the use of stable and radioactive isotopes for determining the concentration of tellurium in body fluids of animals and man, specifically in the blood plasma of rabbits. Particular effort has been devoted to developing a sample-processing technique that allows the total amount of tellurium and isotope ratios to be measured by graphite furnace atomic absorption spectrometry (GFAAS) and secondary ion mass spectrometry (SIMS), respectively. The procedure employed in the SIMS analysis is discussed in detail. Investigations on the plasma clearance and the fractional intestinal absorption were carried out on four rabbits. Tracer solutions containing stable tellurium enriched in 124Te or 126Te and radioactive tellurium (121mTe or 123mTe) were administered by gavage and/or intravenously. Blood samples were drawn during the first 2 days after application. The activity of the separated plasma was measured by standard gamma ray spectrometry. After wet ashing and solvent extraction with MIBK the samples were analyzed for stable tellurium. A detection limit of 1 ng/mL of plasma could be achieved with GFAAS. For SIMS analysis the processed samples were deposited on high-purity graphite backings. Reliable isotope ratios could be determined with sample fractions containing 1 ng of tellurium or even less. The results obtained by applying stable isotopes were found to be in good agreement with the data achieved by using radioactive tracers. Studies on the intestinal absorption and the metabolic behavior of tellurium in human volunteers may thus be performed with stable isotopes.

Animals↗
PubMed1989

Tellurium-induced neuropathy: metabolic alterations associated with demyelination and remyelination in rat sciatic nerve.

Rats fed a diet containing 1.25% elemental tellurium initiated on postnatal day 20 undergo a transient neuropathy characterized by synchronous demyelination of peripheral nerves. In sciatic nerve, the extent of demyelination was maximal after 5 days of tellurium exposure; there was a loss of 25% of the myelin, as assayed by concentration of myelin-specific P0 protein. Tellurium-induced alterations in the metabolic capacity of Schwann cells were examined by measuring the synthesis of myelin lipids in vitro in isolated sciatic nerve segments. Exposure to tellurium resulted in an early marked decrease of approximately 50% in overall incorporation of [14C]acetate into lipids, with a preferential depression in synthesis of cerebrosides, cholesterol, and ethanolamine plasmalogens (components enriched in myelin). Most dramatically, within 1 day of initiation of tellurium exposure, there was a profound increase in [14C]acetate-derived radioactivity in squalene; 23% of incorporated label was in this intermediate of cholesterol biosynthesis, compared to less than 0.5% in controls. In association with the remyelinating phase seen after 5 days of tellurium exposure, synthesis of myelin components gradually returned to normal levels. After 30 days, metabolic and morphologic alterations were no longer apparent. We suggest that the sequence of metabolic events in sciatic nerve following tellurium treatment initially involves inhibition of the conversion of squalene to 2,3-epoxysqualene, and that this block in the cholesterol biosynthesis pathway results, either directly or indirectly, in the inhibition of the synthesis of myelin components and breakdown of myelin.

Acetates↗
PubMed2006

Tellurium adatoms as an in-situ surface probe of (111) two-dimensional domains at platinum surfaces.

Irreversibly adsorbed tellurium has been studied as a probe to quantify ordered domains in platinum electrodes. The surface redox process of adsorbed tellurium on the Pt(111) electrode and Pt(111) stepped surfaces takes place around 0.85 V in a well-defined peak. The behavior of this redox process on the Pt(111) vicinal surfaces indicates that the tellurium atoms involved in the redox process are only those deposited on the (111) terrace sites. Moreover, the corresponding charge density is proportional to the number of sites on (111) ordered domains (terraces) that are, at least, three atoms wide. Hence, this charge density can be used to measure the number of (111) terrace sites on any given platinum sample. Structural information about tellurium adsorption is obtained from atomic-resolution STM images for the Pt(111) and Pt(10, 10, 9) electrodes. A rectangular structure (2 x radical 3) and a compact hexagonal structure (11 x 8) were identified. However, the redox peak for adsorbed tellurium on (100) domains at 1.03 V overlaps with peaks arising from steps and (110) sites. Therefore, it cannot be used without problems for the determination of (100) sites on a platinum sample. On the (100) terraces, the surface structure of the adsorbed tellurium is c(2 x 2), as revealed by STM. Finally, tellurium irreversible adsorption has been used to estimate the number of (111) ordered domains terrace sites on different polycrystalline platinum samples, and the results are compared to those obtained with bismuth irreversible adsorption.

Journal Article↗
PubMed1988

Developmental toxicology investigation of tellurium.

The developmental toxicity of tellurium was evaluated in Crl Sprague-Dawley rats and New Zealand white rabbits by means of standard segment II-type studies. Groups of pregnant rats were fed a diet containing 0, 30, 300, 3000, or 15,000 ppm of tellurium on Days 6 through 15 of gestation (microscopic detection of sperm in a smear of vaginal contents considered as Day 0), and artificially inseminated rabbits were fed a diet containing 0, 17.5, 175, 1750, and 5250 ppm of tellurium during Days 6 through 18 of gestation (day of insemination considered as Day 0). Signs of maternal toxicity were observed during the treatment period in a statistically significant and dose-related manner at dietary concentrations of 300 ppm and greater in rats and 1750 ppm and greater in rabbits. Exposure of these pregnant rats and rabbits to tellurium had no effect upon reproduction as measured by pregnancy rate, litter size, dead or resorbed implantations, or fetal sex ratio. Both skeletal (primarily skeletal maturational delays) and soft tissue malformations (primarily hydrocephalus) were noted in the offspring of pregnant rats exposed to the highest levels (3000 and 15,000 ppm) of tellurium. Rabbit fetuses of the highest dosage group (5250 ppm) had a slightly elevated evidence of skeletal delays and nonspecific abnormalities. Since maternal toxicity was observed at dosages that did not affect the developing conceptus, there were no indications of unique developmental susceptibility upon exposure of pregnant rats or rabbits to tellurium.

Abnormalities, Drug-Induced↗
PubMed1999

Binding of tellurium to hepatocellular selenoproteins during incubation with inorganic tellurite: consequences for the activity of selenium-dependent glutathione peroxidase.

The metallic group XVIa elements selenium and tellurium possess remarkably similar chemical properties. However, unlike selenium, tellurium is not an essential micronutrient and, indeed, induces both acute and chronic toxicity in a variety of species. Despite this, very little is known of the molecular mechanisms of toxicity of tellurium, particularly with respect to potential chemical interactions with selenium-containing components in the cell. In this work we describe a novel interaction of inorganic tellurite with hepatocellular selenoproteins, particularly with selenium-dependent glutathione peroxidase. The accumulation of (121Te)-tellurite into cultured primary rat liver hepatocytes was shown to be much more rapid than that of (75Se)-selenite on a molar basis. Neither the uptake of (121Te)-tellurite nor of (75Se)-selenite was affected by a large molar excess of the unlabelled counterpart, respectively. Interestingly, separation of the hepatocellular proteins on continuous pH denaturing gels demonstrated clear binding of radiolabelled tellurium to a number of protein bands, including one at 23 and one at 58 kDa, which corresponded to proteins readily labelled in cells treated with (75Se)-selenite. The binding of (121Te) to these proteins was insensitive to reduction with mercaptoethanol and not affected by pre-treatment of the cells with cycloheximide. When purified selenium-dependent glutathione peroxidase was treated directly with (121Te)-tellurite, the protein became labelled in an analogous manner to that achieved in intact cells. This was not affected by coincubation of the enzyme with (121Te)-tellurite and one or both of its substrates. Additionally, incubation of the peroxidase with tellurite effectively inhibited its ability to catalyse glutathione-dependent reduction of hydrogen peroxide. These data suggest that inorganic tellurite delivers tellurium to the intracellular milieu in a form capable of binding to some intracellular selenoproteins and at least in the case of glutathione peroxidase, cause inhibition of catalytic activity. The nature of the binding seems not to be due to the insertion of tellurocysteine into the protein and the insensitivity to reductive cleavage with mercaptoethanol seems to preclude the formation of stable telluro-selenides in the proteins. These data may offer alternative explanations for the established toxicity of tellurium via disruption of selenoprotein function, particularly by the induction of intracellular oxidative stress by the inhibition of Se-dependent glutathione peroxidase.

Animals↗
PubMed1983

An analytical method of ultra-trace tellurium for samples of sea- and environmental-water.

This paper presents a method for the concentration of tellurium in sulfhydral cotton fiber. The mechanism of Te-Re catalytic polarographic behaviour has been studied. The optimal conditions of systems are proposed. An analytical procedure of preconcentration with sulfhydral cotton fiber and catalytic polarographic determination of ultra-trace tellurium is presented. This method exhibits good selectivity and is simple and easy. It is also one o;f the most sensitive analytical methods of tellurium at present. The procedure is demonstrated successfully for the determination of background levels of tellurium in a variety of natural water. This is the first reported determination of tellurium in sea water, filling a gap in the literature of oceanic geochemistry. It was found that the content of tellurium in South China sea water is 8 X 10(-10) g/l, that in East China sea water is 4-7 X 10(-10) g/l.

Polarography↗
PubMed2001

Determination of tellurium in indium antimonide semiconductor material by electrothermal atomic absorption spectrometry.

A method for the determination of the dopant concentration of tellurium in dissolved indium antimonide semiconductor material by electrothermal atomic absorption spectrometry (ETAAS) was developed. Efforts were made to investigate the optimal conditions of the furnace heating program and the effect of palladium modifier on the variation of tellurium and the background absorbance. According to the results obtained, the presence of palladium chemical modifier in the analysis of indium antimonide allowed the successful retention of tellurium in the graphite tube, and the optimum mass of palladium modifier was found to be dependent on the sample matrix concentration. The absorbance profile of tellurium and the background level were significantly improved when a pyrolysis temperature of 1100 degrees C and an atomization temperature of 2200 degrees C were employed in the optimized heating program. With the use of this method, a detection limit of 0.8 microg g(-1) tellurium in indium antimonide could be achieved. The applicability of the proposed method was evaluated by comparison with two independent methods, i.e. slurry sampling-ETAAS and ICP-MS. From the good agreement between the results, it was demonstrated that the proposed method is suitable for the determination of typical dopant concentrations of tellurium in indium antimonide.

Journal Article↗
PubMed1993

Evidence for telluroamino acid in biological materials and some rules of assimilation of inorganic tellurium by yeast.

A natural substance, telluroamino acid, was discovered in tellurium yeast by GC and GC/MS. This substance was obtained for the first time by means of the assimilation of inorganic tellurium by yeast, having 600 ppm of total Te and 150 ppm of telluroamino acid. Some rules for such an assimilation were found: the content of total Te and telluroamino acid in tellurium-yeast is closely related to the kind of culture media used and is proportional to the concentration of Te in culture media. This discovery is of theoretical and practical significance, especially for the production by a simpler microbiological synthesis of rare and expensive organic tellurium compounds which hopefully will prove to be anticarcinogens like the selenium-yeast, and for explaining the biochemical effect of tellurium on the human body.

Amino Acids↗
PubMed1991

Primary demyelination induced by exposure to tellurium alters mRNA levels for nerve growth factor receptor, SCIP, 2',3'-cyclic nucleotide 3'-phosphodiesterase, and myelin proteolipid protein in rat sciatic nerve.

Weanling rats fed a diet containing tellurium develop a peripheral neuropathy characterized by a highly synchronous primary demyelination; this demyelination is followed closely by a period of rapid remyelination. The demyelination is related to the inhibition of squalene epoxidase activity, which results in a block in cholesterol synthesis. Expression of mRNA for the major structural proteins of PNS myelin, myelin basic protein and P0, is coordinately down-regulated during the demyelinating phase and then up-regulated during the remyelinating phase (Toews et al., J. Neurosci. Res., 26 (1990) 501-507). We now report tellurium-induced alterations in gene expression for several proteins which are not major structural components of myelin in the peripheral nervous system. Expression of mRNA for nerve growth factor receptor in sciatic nerve was very low in control animals, but was markedly up-regulated after 3-5 days of exposure to tellurium, a time corresponding to the beginning of demyelination. Levels remained elevated during the subsequent period of remyelination. Expression of mRNA for SCIP (a presumptive transcription factor) was also up-regulated in sciatic nerve following tellurium exposure, with a time course similar to that for nerve growth factor receptor. When examined as a fraction of total RNA, steady-state mRNA levels for 2',3'-cyclic nucleotide 3'-phosphodiesterase and the myelin proteolipid protein were decreased during the demyelinating phase; however, this decrease could be largely accounted for by increased levels of total RNA. When analyzed on a 'per nerve' basis, steady-state mRNA levels for these two proteins were actually increased about 2-fold by 9 days after beginning tellurium exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1995

How does garlic exert its hypocholesterolaemic action? The tellurium hypothesis.

The efficacy of garlic as a lipid-lowering agent is being increasingly recognized, but the biochemical mechanisms underlying this action are currently unknown. It is proposed that organic tellurium compounds, which are found in high concentration in fresh garlic buds, may contribute to this action by inhibiting squalene epoxidase, the penultimate enzyme in the synthetic pathway of cholesterol. Weanling rats fed a diet rich in tellurium develop a demyelinating polyneuropathy due to inhibition of this enzyme in peripheral nerves. Chronic exposure to small amounts of tellurium found in garlic might reduce endogenous cholesterol production through inhibition of hepatic squalene epoxidase and so reduce cholesterol levels. Tellurium may also contribute to the characteristic odour of garlic since the most obvious clinical sign of tellurium poisoning is a garlic-like odour.

Animals↗
PubMed1996

Alzheimer's disease, Kuf's disease, tellurium and selenium.

The possible role of the abnormal trace element tellurium in the pathogenesis of Alzheimer's disease is examined. Tellurium has been reported to produce cognitive impairment and cerebral lipofuscinosis in rats-changes akin to those seen in Kuf's disease, a condition which shares certain clinical and neuropathological features with Alzheimer's disease. Tellurium can damage mitochondria; defects in mitochondrial energy metabolism may be relevant to the pathogenesis of neurodegenerative disease. The deficiency of selenium, which may act physiologically as an antagonist of tellurium, in the Alzheimer's disease brain would also be in keeping with the hypothesis of tellurium toxicity as a factor in the pathogenesis of Alzheimer's disease.

Adult↗
PubMed1988

Maternal toxicity and teratogenicity of tellurium dioxide in the Wistar rat: relationship to pair-feeding.

Tellurium dioxide (TeO2) induces hydrocephalus, edema, exophthalmia, ocular hemorrhage, umbilical hernia, undescended testes and small kidneys in day 20 Wistar rat fetuses when administered s.c. to pregnant dams from gestational day 15 to 19. At doses of 500 mumole/kg or greater, a 100% incidence of these findings and a reduction in maternal weight gain were observed. A pair-fed study at the dose of 500 mumole/kg of TeO2 was conducted to establish if the effects of tellurium were a result of a reduction in food intake or other maternal toxic responses. Two additional control groups of rats receiving tellurium or vehicle were fed ad libitum. After a comparable maternal weight gain from day 0 to 15, weight gain was significantly reduced in the treated groups and the pair-fed control. There was a reduction of fetal weight in the treated groups (p less than 0.01) and in the pair-fed control (p less than 0.02). There was a 100% incidence of the above anomalies in the litters of the two treated groups, but none in the pair-fed and control groups. No histological alterations other than a mild centrolobular fatty change in the liver were detected in the other organs from the tellurium exposed dams. Thus, tellurium induces both maternal toxicity and teratogenic effects in the rat where the teratogenicity is not mediated by alterations in the diet.

Abnormalities, Drug-Induced↗
PubMed1992

Selective inhibition of Zn(2+)-glycerophosphocholine cholinephosphodiesterase by tellurium tetrachloride.

A Zn(2+)-glycerophosphocholine cholinephosphodiesterase (EC 3.1.4.38) purified from mouse brain was found to be reversibly inhibited by tellurium tetrachloride. This effect was characterized by a competitive pattern of inhibition, with apparent Ki values of 0.7 microM and 1.5 microM for the hydrolysis of p-nitrophenylphosphocholine and glycerophosphocholine respectively. Interestingly, the inhibitory effect of tellurium tetrachloride was found to be greatly potentiated by tetramethylammonium salt, indicative of a synergistic interaction between the two compounds. Additionally, it was observed that the effect of tellurium tetrachloride was not affected by a number of other metal ions, and was more pronounced at neutral pH, suggesting that the inhibitory role of the tellurium tetrachloride may be of importance under physiological conditions. Thus Zn(2+)-glycerophosphocholine cholinephosphodiesterase is proposed to be one of the target enzymes which is susceptible to the inhibitory effect of tellurium tetrachloride.

Animals↗
PubMed1995

Tellurite specifically affects squalene epoxidase: investigations examining the mechanism of tellurium-induced neuropathy.

A peripheral neuropathy characterized by a transient demyelinating/remyelinating sequence results when young rats are fed a tellurium-containing diet. The neuropathy occurs secondary to a systemic block in cholesterol synthesis. Squalene accumulation suggested the lesion was at the level of squalene expoxidase, a microsomal monooxygenase that uses NADPH cytochrome P450 reductase to receive its necessary reducing equivalents from NADPH. We have now demonstrated directly specificity for squalene epoxidase; our in vitro studies show that squalene epoxidase is inhibited 50% in the presence of 5 microM tellurite, the presumptive in vivo active metabolite. Under these conditions, the activities of other monooxygenases, aniline hydroxylase and benzo(a)pyrene hydroxylase, were inhibited less than 5%. We also present data suggesting that tellurite inhibits squalene epoxidation by interacting with highly susceptible -SH groups present on this monooxygenase. In vivo studies of specificity were based on the compensatory response to feeding of tellurium. Following tellurium intoxication, there was up-regulation of squalene epoxidase activity both in liver (11-fold) and sciatic nerve (fivefold). This induction was a specific response, as demonstrated in liver by the lack of up-regulation following exposure to the nonspecific microsomal enzyme inducer, phenobarbital. As a control, we also measured the microsomal monooxygenase activities of aniline hydroxylase and benzo(a)pyrene hydroxylase. Although they were induced following phenobarbital exposure, activities of these monooxygenases were not affected following tellurium intoxication, providing further evidence of specificity of tellurium intoxication for squalene epoxidase.

Aniline Hydroxylase↗
PubMed1991

Tellurium blocks cholesterol synthesis by inhibiting squalene metabolism: preferential vulnerability to this metabolic block leads to peripheral nervous system demyelination.

Inclusion of 1.1% elemental tellurium in the diet of postweanling rats produces a peripheral neuropathy due to a highly synchronous primary demyelination of sciatic nerve; this demyelination is followed closely by remyelination. Sciatic nerves from animals fed tellurium for various times were removed and incubated ex vivo for 1 h with [14C]acetate, and radioactivity incorporated into individual lipid classes was determined. In nerves from rats exposed to tellurium, there was a profound and selective block in the conversion of radioactive acetate to cholesterol. Another radioactive precursor, [3H]water, gave similar results. We suggest that tellurium feeding inhibits squalene epoxidase activity and that the consequent lack of cholesterol destabilizes myelin, thereby causing destruction of the larger internodes. Ex vivo incubation experiments were also carried out with liver slices. As with nerve, tellurium feeding caused accumulation in squalene of label from radioactive acetate, whereas labeling of cholesterol was greatly inhibited. Unexpectedly, however, incorporation of label from [3H]water into both squalene and cholesterol was increased. Relevant is the demonstration that liver was the primary site of bulk accumulation of squalene, which accounted for 10% of liver dry weight at 5 days. Thus, accumulation of squalene (and other mechanisms, possibly including up-regulation of cholesterol biosynthetic pathways) drives squalene epoxidase activity at normal levels in liver even in the presence of inhibitors of this enzyme. This is reflected by continuing incorporation of [3H]water into cholesterol; incorporation of this precursor takes place at many of the postsqualene biosynthetic steps for sterol formation. [14C]Acetate entering the sterol pathway before squalene in liver is greatly diluted in specific activity when it reaches the large squalene pool, and thus increased squalene epoxidase activity does not transfer significant 14C label to sterols. In contrast to the situation with liver, synthesis of sterols is markedly depressed in sciatic nerve, and squalene does not accumulate to high levels.

Acetates↗
PubMed2005

Acute tellurium toxicity from ingestion of metal-oxidizing solutions.

Tellurium is an element used in the vulcanization of rubber and in metal-oxidizing solutions to blacken or tarnish metals. Descriptions of human toxicity from tellurium ingestion are rare. We report the clinical course of 2 children who ingested metal-oxidizing solutions containing substantial concentrations of tellurium. Clinical features included vomiting, black discoloration of the oral mucosa, and a garlic odor to the breath. One patient developed corrosive injury to the esophagus secondary to the high concentration of hydrochloric acid in the solution. Both patients recovered without serious sequelae, which is typical of tellurium toxicity. An awareness of situations in which children may be exposed to tellurium and its clinical presentation may assist clinicians in the diagnosis of this rare poisoning.

Acute Disease↗
PubMed2004

Simultaneous determination of bismuth and tellurium in steels by high power nitrogen microwave induced plasma atomic emission spectrometry coupled with the hydride generation technique.

An annular-shaped, high power nitrogen microwave induced plasma (N(2)-MIP) produced at atmospheric pressure by an Okamoto cavity, as a new excitation source for atomic emission spectrometry (AES), has been used for the simultaneous determination of bismuth and tellurium in steels with the hydride generation method. Under the optimized experimental conditions, the best attainable detection limits at the Bi I 195.389 nm and Te I 200.200 nm lines were 110 and 86 ng/ml for bismuth and tellurium, respectively. The linear dynamic ranges for bismuth and tellurium were 300 to 30,000 ng/ml. The presence of several diverse elements was found to cause a more or less depressing interference with the proposed technique. When bismuth and tellurium in steels were determined, a large amount of Fe(III) in the solution caused a severe depressing interference, while the presence of Fe(II) showed little or no significant interference. Of the several interference-releasing agents examined, l-ascorbic acid was found to be the most preferable to reduce Fe(III) to Fe(II) prior to hydride generation. The concentrations of bismuth and tellurium in steels were determined by the proposed technique. The results obtained by this method were in good agreement with their certified values.

Journal Article↗