Acute tellurium toxicity from ingestion of metal-oxidizing solutions.
ABSTRACT 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.
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ABSTRACT: The objective of this investigation was to predict the toxic properties of Sodium tellurite against selected human pathogens. A group of six human bacterial pathogens Staphylococcus aureus, Strepto pyogenes, Bacillus subtilis, Proteus vulgaris, Escherichia coli and Klebsiella planticola were utilized for screening. The spectrum of toxic properties was compared by means formation of zone. Our study demonstrated that sodium tellurite exhibit a strong toxic effect on B. subtilis (30±2mm), P. vulgaris (27 ± 2 mm) and S. aureus (25 ± 0.5 mm). The activity was compared with standard Ciprofloxacin disc (5µg/disc) and the zone of inhibition was 24 ± 1.4 mm. However, Gram negative bacteria exhibited resistance to Sodium tellurite except proteus vulgaris that we screened in our study. Our study suggested that the anti bacterial effect of sodium tellurite is not wider spectrum but selectively more significant even when compared with standard Ciprofloxacin.Research Journal of Pharmacy and Technology 05/2014; 7(5):499-501.
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ABSTRACT: Anxiety-related disorders are a common public health issue. Several lines of evidence suggest that altered glutamatergic neurotransmission underlies anxiety. The present study evaluated the effect of diphenyl ditelluride [(PhTe)2] exposure on the behavioral performance of rats and examined whether the behavioral effects could be attributed to changes in the modulation of glutamatergic function. Rats were exposed to (PhTe)2 (subcutaneously) during 8 weeks-final dose one third LD50 (124 μg/kg). The testing schedule included elevated plus-maze, open-field, T-maze, rotorod, and Morris water maze tests. Synaptosomal basal [(3)H] glutamate release and uptake were also evaluated. The time spent in the open arm and the ratio of time spent in the open arm/total were decreased in the (PhTe)2 group. Furthermore, the [(3)H] glutamate uptake was decreased in this experimental group. The results suggest that exposure to (PhTe)2 did not change motor abilities whereas it may result in anxiogenic-like behavior, induced by changes in the glutamatergic system at the pre-synaptic level.Biological trace element research 04/2014; DOI:10.1007/s12011-014-9960-4 · 1.92 Impact Factor
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ABSTRACT: 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 Ca(2+) 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 Ca(2+)-mediated mechanisms in developmental rat brain. We propose that the disrupted cytoskeletal homeostasis could support brain damage provoked by this neurotoxicant.Oxidative medicine and cellular longevity 01/2014; 2014:458601. DOI:10.1155/2014/458601 · 3.36 Impact Factor