The tellurium content of vegetation

Vegetation growing in the Ely mining district of White Pine County, NV has been analyzed for tellurium to discover whether Te accumulator plants existed similar to those that take up Se in great quantities. In addition, the variation in Te content among species growing in different geological settings was studied. Another objective of this study was to determine the range of Te concentration in vegetation in regions where the Te content of surface materials was high, as in the Ely mining district, and low as in various areas of western CO. Trees and shrubs (480 samples) as well as flowering plants (505 samples) and their associated edaphic materials were collected from six sites in the Ely region and all plant parts were analyzed for Te, Se, Fe, S, Zn, Cu, and Pb. One hundred and five plants were collected from three areas in western CO. There is a highly significant difference between Te uptake by trees and that of perennial flowering plants. Flowers contain significantly more Te on the average than other plant parts. An examination of the Te content of tree parts reveals that leaves sorb the most and branches the least. When the Te content of edaphic materials is high, there is a corresponding increase in the Te content of plants. Shallow perennial plants were not found growing in areas where soils contained more than 10 mg kg⁻¹ Te. Seleniferous species ofAstragalus contain larger quantities of Te than plants in the Ely area, whereas nonseleniferous members of this genus contain much less. The nitrotoxin producing Astragali contain concentrations of Te greater than that encountered in nonseleniferous species but less than that in seleniferous ones. No plants contained more than 1 mg kg⁻¹ Te. Iron, Te, Se, and S are coherent in all plants and in most soils and rocks examined.     

Sulfur,selenium and tellurium containing amines act as effective carbonic anhydrase activators

A new series of β-aminochalcogenides were designed and synthesized to identify new carbonic anhydrase activator (CAA) agents as novel tools for the management of several neurodegenerative and metabolic disorders which represent a clinical challenge without effective therapies available. Some β-aminoselenides and β-aminotellurides showed effective CA activating effects and a potent antioxidant activity. CAAs may have applications for memory therapy and CA deficiency syndromes.     

钝顶螺旋藻对无机碲的吸收代谢作用

研究钝顶螺旋藻对无机碲的吸收代谢作用,在钝顶螺旋藻稳定生长期(7d、8d、9d)添加700～1000 mg·L~(-1)的亚碲酸钠。结果表明,钝顶螺旋藻对无机碲有良好的有机化作用,其有机化比率达到75～80%;藻体中不同组分(固体残余物、水溶性蛋白、非蛋白水溶性物质)均有结合碲,这些组分主要是水溶性蛋白。此外,气态碲的产量和产率均随着碲剂量的增大而增加,当碲的累计浓度为1000mg·L~(-1)时,培养液中无机碲的残余率为48%,表明钝顶螺旋藻在生物修复碲污染方面有很大的开发应用潜力。     

First evaluation of organotellurium derivatives as carbonic anhydrase I,II, IV,VII and IX inhibitors

A series of tellurides was evaluated as carbonic anhydrase (CA, EC 4.2.1.1) inhibitors against the human (h) carbonic anhydrase isoforms hCA I, II, IV, VII and IX, involved in a variety of diseases, including glaucoma, retinitis pigmentosa, epilepsy, arthritis and tumors. These compounds, which are the first tellurium-containing derivatives acting as inhibitors of carbonic anhydrase enzymes, showed effective inhibition against all isoforms investigated and some of them were selective for inhibiting the cytosolic or the membrane-bound CAs. Thus, these carbonic anhydrase inhibitors are interesting leads for the development of isoform-selective inhibitors.     

Sulfur,selenium and tellurium pseudopeptides: Synthesis and biological evaluation

A new series of sulfur, selenium and tellurium peptidomimetic compounds was prepared employing the Passerini and Ugi isocyanide based multicomponent reactions (IMCRs). These reactions were clearly superior to conventional methods traditionally used for organoselenium and organotellurium synthesis, such as classical nucleophilic substitution and coupling methods. From the biological point of view, these compounds are of considerable interest because of suspected anticancer and antimicrobial activities. While the sulfur and selenium containing compounds generally did not show either anticancer or antimicrobial activities, their tellurium based counterparts frequently exhibited antimicrobial activity and were also cytotoxic. Some of the compounds synthesized even showed selective activity against certain cancer cells in cell culture. These compounds induced a cell cycle delay in the G0/G1 phase. At closer inspection, the ER and the actin cytoskeleton appeared to be the primary cellular targets of these tellurium compounds, in line with some of our previous studies. As most of these peptidomimetic compounds also comply with Lipinski’s Rule of Five, they promise good bioavailability, which needs to be studied as part of future investigations.     

Alterations in Gene Expression Associated with Primary Demyelination and Remyelination in the Peripheral Nervous System

Primary demyelination is an important component of a number of human diseases and toxic neuropathies. Animal models of primary demyelination are useful for isolating processes involved in myelin breakdown and remyelination because the complicating events associated with axonal degeneration and regeneration are not present. The tellurium neuropathy model has proven especially useful in this respect. Tellurium specifically blocks synthesis of cholesterol, a major component of PNS myelin. The resulting cholesterol deficit in myelin-producing Schwann cells rapidly leads to synchronous primary demyelination of the sciatic nerve, which is followed by rapid synchronous remyelination when tellurium exposure is discontinued. Known alterations in gene expression for myelin proteins and for other proteins involved in the sequence of events associated with demyelination and subsequent remyelination in the PNS are reviewed, and new data regarding gene expression changes during tellurium neuropathy are presented and discussed.     

Human erythrocyte hemolysis induced by selenium and tellurium compounds increased by GSH or glucose: a possible involvement of reactive oxygen species

Oxidative stress can induce complex alterations of membrane proteins in red blood cells (RBCs) eventually leading to hemolysis. RBCs represent a good model to investigate the damage induced by oxidizing agents. Literature data have reported that chalcogen compounds can present pro-oxidant properties with potent inhibitory effects on cell growth, causing tissue damage and inhibit a variety of enzymes. In this study, human erythrocytes were incubated in vitro with various chalcogen compounds at 37 °C: diphenyl ditelluride (1), dinaphthalen diteluride (2), diphenyl diselenide (3), (S)-tert-butyl 1-diselenide-3-methylbutan-2-ylcarbamate (4), (S)-tert-butyl 1-diselenide-3-phenylpropan-2-ylcarbamate (5), selenium dioxide (6) and sodium selenite (7) in order to investigate their potential in vitro toxicity. After 6 h of incubation, all the tested compounds increased the hemolysis rate, when compared to control and compound (2) had the most potent hemolytic effect. The addition of reduced glutathione (GSH) or glucose to the incubation medium enhanced hemolysis caused by chalcogen compounds. The thiol oxidase activity of these compounds was evaluated by measuring the rate of cysteine (CYS) and dithiotreitol (DTT) oxidation. DTT and cysteine oxidation was increased by all the compounds tested. The results suggest a relationship between the oxidation of intracellular GSH and subsequent generation of free radicals with the hemolysis by chalcogen compounds.     

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.     

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.     

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.