Acute tellurium toxicity from ingestion of metal-oxidizing solutions
The University of Arizona, Tucson, Arizona, United StatesPEDIATRICS (Impact Factor: 5.47). 09/2005; 116(2):e319-21. DOI: 10.1542/peds.2005-0172
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.
- "However, toxicity of tellurium compounds largely depends on the chemical form and the quantity of the element consumed. Tellurium showed acute toxicity in young children when ingestion of metal-oxidizing solutions containing signifi cant concentrations of Te (Yarema andCurry 2005, Taylor 1996). Tellurium can be accumulated in the kidney, heart, liver, spleen and muscle and its content in liver and the kidney in excess of 0.002 g kg −1 (Chai and Zhu 1994). "
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- "But to date, no telluroproteins have been identified in animal cells. Nowadays, two cases of toxicity in young children from ingestion of metal-oxidizing solutions that contained substantial concentrations of Te were reported in the literature (Yarema and Curry, 2005). Clinical features of acute Te toxicity include a metallic taste, nausea, blackened oral mucosa and skin and garlic odor of the breath (Muller et al., 1989; Taylor, 1996). "
ABSTRACT: In the present report we examined the effect of maternal exposure to diphenyl ditelluride (PhTe)(2) (0.01mg/kg body weight) during the first 14 days of lactational period on the activity of some protein kinases targeting the cytoskeleton of striatum and cerebellum of their offspring. We analyzed the phosphorylating system associated with glial fibrillary acidic protein (GFAP), and neurofilament of low, medium and high molecular weight (NF-L, NF-M and NF-H, respectively) of pups on PND 15, 21, 30 and 45. We found that (PhTe)(2) induced hyperphosphorylation of all the proteins studied on PND 15 and 21, recovering control values on PND 30 and 45. The immunocontent of GFAP, NF-L, NF-M and NF-H in the cerebellum of 15-day-old pups was increased. Western blot assays showed activation/phosphorylation of Erk1/2 on PND 21 and activation/phosphorylation of JNK on PND 15. Otherwise, p38MAPK was not activated in the striatum of (PhTe)(2) exposed pups. On the other hand, the cerebellum of pups exposed to (PhTe)(2) presented activated/phosphorylated Erk1/2 on PND 15 and 21 as well as activated/phosphorylated p38MAPK on PND 21, while JNK was not activated. Western blot assays showed that both in the striatum and in the cerebellum of (PhTe)(2) exposed pups, the immunocontent of the catalytic subunit of PKA (PKAcα) was increased on PND 15. Western blot showed that the phosphorylation level of NF-L Ser55 and NF-M/NF-H KSP repeats was increased in the striatum and cerebellum of both 15- and 21-day-old pups exposed to (PhTe)(2). Diphenyl diselenide (PhSe)(2), the selenium analog of (PhTe)(2), prevented (PhTe)(2)-induced hyperphosphorylation of striatal intermediate filament (IF) proteins but it failed to prevent the action of (PhTe)(2) in cerebellum. Western blot assay showed that the (PhSe)(2) prevented activation/phosphorylation of Erk1/2, JNK and PKAcα but did not prevent the stimulatory effect of (PhTe)(2) on p38MAPK in cerebellum at PND 21. In conclusion, this study demonstrated that dam exposure to low doses of (PhTe)(2) can alter cellular signaling targeting the cytoskeleton of striatum and cerebellum in the offspring in a spatiotemporal manner, which can be related to the neurotoxic effects of (PhTe)(2).
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- "Nowadays due to the importance of the chirality in biological processes, racemic organochalcogen compounds are hardly considered for synthetic purposes (Petragnani and Stefani, 2007; Gotor et al., 2008). In this context, Tellurium (Te) compounds have been used or produced in various industrial processes such as: electronic industry, gasoline antiknock additive (Fairhill, 1969) and byproduct from the electrolytic refining of copper (Yarema and Curry, 2005). Te compounds can cause poisoning which leads to clinical features including a metallic taste, nausea, blackened oral mucosa and skin, and garlic odor of the breath (Muller et al., 1989). "
ABSTRACT: Organotellurium compounds have been synthesized since 1840, but their pharmacological and toxicological properties are still incipient. Therefore, the objective of this study was to verify the effect of acute administration with the organochalcogen 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on the activity of brain creatine kinase (CK), a key enzyme in energy metabolism, and on behaviors in the open field test of 30-day-old rats. Animals were treated intraperitoneally with a single dose of the organotellurium (125, 250, or 500 μg/kg body weight) and after 55 min of the drug administration the open field test was carried out. Behavior analyses were performed during 5 min and the number of the squares crossed, number of rearing, number of groomings and number of fecal boli were recorded by an observer. Then, the animals were sacrificed and the cerebral cortex, the hippocampus, and the cerebellum were dissected, and CK activity and sulfhydryl content were measured in the brain. The organotellurium increased the ambulation and rearing behaviors in the open field test at doses of 250 and 500 μg/kg. Moreover, the compound inhibited CK activity and provoked a reduced of thiol content measured by the sulfhydryl assay in all the tissues studied. Therefore, changes in energy homeostasis and motor behavior in rats treated with this organotellurium support the hypotheses that the brain is a potential target to pharmacological and toxicological effects of this compound.
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