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Health effects of tellurium
Fortunately, tellurium compounds are encountered rarely by most people. They are teratogenic and should only be handled by competent chemists since ingestion in even small amounts causes dreadful smelling breath and appalling body odour.
Routes of exposure: The substance can be absorbed into the body by inhalation of its aerosol.
Inhalation risk: Evaporation at 20°C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed. Effects of inhalation: Drowsiness. Dry mouth. Metal taste. Headache. Garlic odour. Nausea.
Effects of short-term exposure: The aerosol of this substance irritates the eyes and the respiratory tract. The substance may cause effects on the liver and central nervous system. Exposure may result in garlic-like breath. Medical observation is indicated. Ingestion: Abdominal pain. Constipation. Vomiting.
Chemical dangers: Upon heating, toxic fumes are formed. Reacts vigorously with halogens or interhalogens causing fire hazard. Reacts with zinc with incandescence. Lithium silicide attacks tellurium with incandescence. Combustible. Finely dispersed particles form explosive mixtures in air.
Environmental effects of tellurium
Not harmful or readily rendered harmless by natural processes.
When heated to decomposition, tellurium chloride may emit toxic fumes of tellurium and chlorine.
Toxicol In Vitro. 2004 Aug;18(4):475-82. Related Articles, Links
Organotellurium compound toxicity in a promyelocytic cell line compared to non-tellurium-containing organic analog.
Sailer BL, Liles N, Dickerson S, Sumners S, Chasteen TG.
Department of Biological Sciences, Sam Houston State University, Box 2116, Huntsville, TX 77341-2116, USA. email@example.com
Two substituted aryl organotellurium compounds and a tellurium-free analog of one of these were evaluated for in vitro cytotoxicity using human promyelocytic (HL-60) cells as an experimental system. Both tellurium-containing toxicants (2,2(')-dimethoxydiphenyl ditelluride and 2,2(')-diamino-3,3('),5,5(')-tetramethyldiphenyl ditelluride) were cytotoxic at concentrations as low as 5 x 10(-6) M and the dimethoxydiphenyl compound produced significant numbers of apoptotic cells at a concentration of only 1 x 10(-6) M after 8 h. Data indicate that 2,2(')-dimethoxydiphenyl ditelluride and 2,2(')-diamino-3,3('),5,5(')-tetramethyldiphenyl ditelluride induce apoptosis in both a time and dose dependent manner; however, 2,2(')-dimethoxybiphenyl, structurally comparable to the first of these but without the tellurium bridge, did not produce apoptosis under the concentrations and time course studied. Therefore the telluride moiety was apparently an important factor in the apoptotic effect.
Neurochem Res. 1997 Oct;22(10):1271-80. Related Articles, Links
Alterations in gene expression associated with primary demyelination and remyelination in the peripheral nervous system.
Toews AD, Hostettler J, Barrett C, Morell P.
Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill 27599, USA. ARREL@CSS.UNC.EDU
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 sychronous 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.
Neurotoxicology. 1996 Fall-Winter;17(3-4):685-95. Related Articles, Links
Schwann cells as targets for neurotoxicants.
Morell P, Toews AD.
Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill 27599, USA.
Schwann cells subserve a variety of roles in the peripheral nervous system (PNS), including ionic homeostasis, and protection and possible metabolic support of axons. It is, however, the myelinating subtype of these glia which appear most sensitive to toxic insults. Myelinating Schwann cells must synthesize large amounts of myelin proteins (P0 is the major myelin protein) and lipids (cholesterol is most prominent) within a short, tightly-programmed developmental window. Schwann cells are preferentially vulnerable to neurotoxic insults during this period of maximal metabolic stress. The hydrophobicity of myelin (reservoir for lipid-soluble toxicants) and possible specialized energy-requiring mechanisms for maintenance of myelin structure are points of vulnerability for the mature myelin sheath. Fortunately, Schwann cells are highly plastic; they dedifferentiate to more primitive precursor cells following a demyelinating insult, but are able to redifferentiate and remyelinate axons during subsequent nerve regeneration. For study of such processes, a useful model system is exposure of developing rats to the element tellurium; this produces a highly synchronous primary demyelination of PNS which is followed closely by rapid remyelination. Interpretation of the metabolic events involved in simplified by the nearly complete lack of axonal degeneration. We have uncovered the primary lesion (block in cholesterol biosynthesis) and elucidated some of the steps involved in the demyelination-remyelination response. Particularly useful have been studies of gene expression of certain proteins (nerve growth factor receptor, myelin proteins, macrophage-specific lysozyme) which have enabled us to define some of the cellular responses to this toxicant-induced injury. A generally applicable result that has emerged from these and other similar studies is that upregulation of NGF-R mRNA is a sensitive marker of nerve damage; it may be useful as a screen for potentially neurotoxic compounds.
Ann N Y Acad Sci. 2003 Dec;1010:659-66. Related Articles, Links
Tellurium compound AS101 induces PC12 differentiation and rescues the neurons from apoptotic death.
Makarovsky D, Kalechman Y, Sonino T, Freidkin I, Teitz S, Albeck M, Weil M, Geffen-Aricha R, Yadid G, Sredni B.
C.A.I.R. Institute, Faculty of Life Science, Bar Ilan University, Ramat Gan, 59200 Israel.
Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra (SN). Studies show that anti-apoptotic and neurotrophic agents are suitable candidates to prevent delayed cell death and/or restore neural function. Here we present the nontoxic immunomodulating compound AS101, which has the ability to induce neurite outgrowth and neural differentiation in PC12 cells. The present study shows that components of the ras signaling pathway are crucial for AS101-induced PC12 differentiation. These include p21ras and its downstream effectors, c-raf-1 and MEK, as well as PI3K. Moreover, these components mediate AS101-induced upregulation of p21waf, which is obligatory for AS101-induced PC12 differentiation. Furthermore, nitric oxide plays a significant role in these AS101 activities. Finally, we show that AS101 prevents apoptosis of NGF-differentiated PC12 cells after NGF withdrawal. Taken together, these results suggest that AS101 induces PC12 cell differentiation and survival by activating the ras-ERK1/2 and ras-PI3K signal transduction pathways, as well as inducing NO production. Our findings may be important in understanding the regulation of survival/apoptosis of neurons deprived of neurotropic support. Futhermore the data propose that AS101 may have clinical potential in the treatment of neurodegenerative disorders like Parkinson's disease.
Can J Microbiol. 2001 Jan;47(1):33-40. Related Articles, Links
Glutathione is a target in tellurite toxicity and is protected by tellurite resistance determinants in Escherichia coli.
Turner RJ, Aharonowitz Y, Weiner JH, Taylor DE.
Structural Biology Research Group, Department Biological Sciences, University of Calgary, Calgary, AB T2N 1N4, Canada. firstname.lastname@example.org
Tellurite (TeO3(2-)) is highly toxic to most microorganisms. The mechanisms of toxicity or resistance are poorly understood. It has been shown that tellurite rapidly depletes the reduced thiol content within wild-type Escherichia coli. We have shown that the presence of plasmid-borne tellurite-resistance determinants protects against general thiol oxidation by tellurite. In the present study we observe that the tellurite-dependent depletion of cellular thiols in mutants of the glutathione and thioredoxin thiol:redox system was less than in wild-type cells. To identify the type of low-molecular-weight thiol compounds affected by tellurite exposure, the thiol-containing molecules were analyzed by reverse phase HPLC as their monobromobimane derivatives. Results indicated that reduced glutathione is a major initial target of tellurite reactivity within the cell. Other thiol species are also targeted by tellurite, including reduced coenzyme A. The presence of the tellurite resistance determinants kilA and ter protect against the loss of reduced glutathione by as much as 60% over a 2 h exposure. This protection of glutathione oxidation is likely key to the resistance mechanism of these determinants. Additionally, the thiol oxidation response curves were compared between selenite and tellurite. The loss of thiol compounds within the cell recovered from selenite but not to tellurite.
J Bacteriol. 2004 Mar;186(6):1579-90. Related Articles, Links
Role of a cysteine synthase in Staphylococcus aureus.
Lithgow JK, Hayhurst EJ, Cohen G, Aharonowitz Y, Foster SJ.
Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield S10 2TN, United Kingdom.
The gram-positive human pathogen Staphylococcus aureus is often isolated with media containing potassium tellurite, to which it has a higher level of resistance than Escherichia coli. The S. aureus cysM gene was isolated in a screen for genes that would increase the level of tellurite resistance of E. coli DH5alpha. The protein encoded by S. aureus cysM is sequentially and functionally homologous to the O-acetylserine (thiol)-lyase B family of cysteine synthase proteins. An S. aureus cysM knockout mutant grows poorly in cysteine-limiting conditions, and analysis of the thiol content in cell extracts showed that the cysM mutant produced significantly less cysteine than wild-type S. aureus SH1000. S. aureus SH1000 cannot use sulfate, sulfite, or sulfonates as the source of sulfur in cysteine biosynthesis, which is explained by the absence of genes required for the uptake and reduction of these compounds in the S. aureus genome. S. aureus SH1000, however, can utilize thiosulfate, sulfide, or glutathione as the sole source of sulfur. Mutation of cysM caused increased sensitivity of S. aureus to tellurite, hydrogen peroxide, acid, and diamide and also significantly reduced the ability of S. aureus to recover from starvation in amino acid- or phosphate-limiting conditions, indicating a role for cysteine in the S. aureus stress response and survival mechanisms.