Acute Tellurium Toxicity From Ingestion of Metal-Oxidizing Solutions

Yarema, Mark; Curry, Steven C.

doi:10.1542/peds.2005-0172

Cited by 61 publications

(23 citation statements)

References 6 publications

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“…These solutions are normally used to clean silver objects [87] and were accidentally ingested by the children. Clinical signals of intoxication included vomiting, black discoloration of the oral mucosa, and garlic odor to the breath, which in one of the young children persisted for several months after the intoxication.…”

Section: Cases Of Human Exposure To Telluriummentioning

confidence: 99%

“…Clinical signals of intoxication included vomiting, black discoloration of the oral mucosa, and garlic odor to the breath, which in one of the young children persisted for several months after the intoxication. The presence of garlic odor, though not a definitive clinical signal of tellurium exposure, should be considered as an important clinical feature by the health agents and may assist clinicians in the diagnosis of rare tellurium poisoning [87]. Two postgraduates investigating the potential therapeutic or industrial use of tellurium esters were exposed to tellurium hexafluoride gas in the laboratory [88].…”

Section: Cases Of Human Exposure To Telluriummentioning

confidence: 99%

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Signaling Mechanisms and Disrupted Cytoskeleton in the Diphenyl Ditelluride Neurotoxicity

Pessoa-Pureur

Heimfarth

Rocha

2014

Oxidative Medicine and Cellular Longevity

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Evidence from our group supports that diphenyl ditelluride (PhTe)2 neurotoxicity depends on modulation of signaling pathways initiated at the plasma membrane. The (PhTe)2-evoked signal is transduced downstream of voltage-dependent Ca2+ channels (VDCC), N-methyl-D-aspartate receptors (NMDA), or metabotropic glutamate receptors activation via different kinase pathways (protein kinase A, phospholipase C/protein kinase C, mitogen-activated protein kinases (MAPKs), and Akt signaling pathway). Among the most relevant cues of misregulated signaling mechanisms evoked by (PhTe)2 is the cytoskeleton of neural cells. The in vivo and in vitro exposure to (PhTe)2 induce hyperphosphorylation/hypophosphorylation of neuronal and glial intermediate filament (IF) proteins (neurofilaments and glial fibrillary acidic protein, resp.) in different brain structures of young rats. Phosphorylation of IFs at specific sites modulates their association/disassociation and interferes with important physiological roles, such as axonal transport. Disrupted cytoskeleton is a crucial marker of neurodegeneration and is associated with reactive astrogliosis and apoptotic cell death. This review focuses the current knowledge and important results on the mechanisms of (PhTe)2 neurotoxicity with special emphasis on the cytoskeletal proteins and their differential regulation by kinases/phosphatases and Ca2+-mediated mechanisms in developmental rat brain. We propose that the disrupted cytoskeletal homeostasis could support brain damage provoked by this neurotoxicant.

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Section: Cases Of Human Exposure To Telluriummentioning

confidence: 99%

Section: Cases Of Human Exposure To Telluriummentioning

confidence: 99%

Signaling Mechanisms and Disrupted Cytoskeleton in the Diphenyl Ditelluride Neurotoxicity

Pessoa-Pureur

Heimfarth

Rocha

2014

Oxidative Medicine and Cellular Longevity

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“…In particular, acute oral toxicity tests performed on rats have determined the median lethal dose (LD50) for CdTe to be greater than 2,000 mg/kg, which marks it as not only less toxic than metallic cadmium (Zayed and Philippe 2009), but also considerably less so than cadmium oxide, for which the oral LD50 in rats is 72 mg/kg (Merck 2006). Studies on the toxicity of tellurium are scarce; the element itself appears to be only mildly toxic and not carcinogenic (Harrison et al 1998); Yarema and Curry reported that two subjects intoxicated through accidental ingestion of solutions containing substantial concentrations of tellurium dioxide recovered without serious sequelae (Yarema and Curry 2005).…”

Section: Introductionmentioning

confidence: 99%

Potential Cd emissions from end-of-life CdTe PV

Raugei

Isasa

Palmer

2011

Int J Life Cycle Assess

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Purpose Cadmium telluride photovoltaics (CdTe PV) have grown considerably in the last few years and are now a mainstream energy technology. Concern has been voiced regarding the potential impact caused by the dispersal of the Cd contained in the modules after they are decommissioned. This study presents a new comprehensive analysis of the end-of-life of CdTe PV and reports on the associated Cd emissions to air and water. Methods Three end-of-life scenarios were considered for CdTe PV. In the first one, 100% of the modules are collected and sent to recycling; in the other two, 85% of the modules are recycled, and the rest are assumed to be either treated as normal municipal solid waste or pre-selected and sent to landfills. All input and output data for module decommissioning and recycling were based on the information directly provided by the world-leading CdTe PV manufacturer (First Solar). The inventory modelling was performed with the GaBi life cycle analysis software package in conjunction with the Ecoinvent v.2 database. Results and discussion In all scenarios, end-of-life Cd emissions from CdTe PV were found to be relatively low, for instance when compared to those from NiCd batteries, when expressed per kilogram of Cd content. Conclusions The on-going growth of CdTe PV is unlikely to produce a worrisome increase in the overall Cd emissions to the environment; principally thanks to the expected stringent control of the related Cd-containing waste flows.

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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).…”

Section: Introductionmentioning

confidence: 99%

Acute treatment with the organochalcogen 3‐butyl‐1‐phenyl‐2‐(phenyltelluro)oct‐en‐1‐one produces behavioral changes and inhibition of creatine kinase activity in the brain of rats

Funchal

Andrade

Turcatel

et al. 2011

Intl J of Devlp Neuroscience

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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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Acute Tellurium Toxicity From Ingestion of Metal-Oxidizing Solutions

Abstract: ABBREVIATIONS. HR, heart rate; RR, respiratory rate; BP, blood pressure.

Cited by 61 publications

References 6 publications

Signaling Mechanisms and Disrupted Cytoskeleton in the Diphenyl Ditelluride Neurotoxicity

Signaling Mechanisms and Disrupted Cytoskeleton in the Diphenyl Ditelluride Neurotoxicity

Potential Cd emissions from end-of-life CdTe PV

Acute treatment with the organochalcogen 3‐butyl‐1‐phenyl‐2‐(phenyltelluro)oct‐en‐1‐one produces behavioral changes and inhibition of creatine kinase activity in the brain of rats

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