Triethyltin

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Mauro Panunzio - One of the best experts on this subject based on the ideXlab platform.

Sha Long - One of the best experts on this subject based on the ideXlab platform.

Alessandro Bongini - One of the best experts on this subject based on the ideXlab platform.

Rosa Cristofol - One of the best experts on this subject based on the ideXlab platform.

  • neurotoxic effects of trimethyltin and Triethyltin on human fetal neuron and astrocyte cultures a comparative study with rat neuronal cultures and human cell lines
    Toxicology Letters, 2004
    Co-Authors: Rosa Cristofol, Sergi Gasso, David Vilchez, Maria Pertusa, E Rodriguezfarre, Coral Sanfeliu
    Abstract:

    Abstract Trimethyltin (TMT) and Triethyltin (TET) caused cell death in cultures of primary human neurons and astrocytes, rat neurons and human neuroblastoma cell lines. Human neurons and astrocytes showed a delayed response to TMT cytotoxicity. After 24 h of TMT exposure, LC50 values were 148.1, 335.5 and 609.7 μM for SK-N-MC neuroblastoma cell line, neurons and astrocytes, respectively. Over 5 days of exposure, the cytotoxic potency of TMT increased about 70-fold in human cortical neurons. Rat hippocampal neurons were the most vulnerable cells to TMT cytotoxicity, exhibiting an LC50 value 30-fold lower (1.4 μM) than that of rat cerebellar granule cells (44.28 μM). With the exception of rat hippocampal neurons, TET was more potent than TMT in inducing cell death (LC50 values of 3.5–16.9 μM). Moreover, TET was more effective than TMT in increasing intracellular free Ca2+ concentration in human and rat neurons. This work shows that human fetal neuron and astrocyte cultures are a useful model for studying the neurotoxic effects of these environmental contaminants and, thus, predicting their impact on human health.

  • trimethyltin and Triethyltin differentially induce spontaneous noradrenaline release from rat hippocampal slices
    Toxicology and Applied Pharmacology, 2000
    Co-Authors: Sergi Gasso, E Rodriguezfarre, Coral Sanfeliu, Cristina Sunol, Rosa Cristofol
    Abstract:

    The environmental contaminants trimethyltin (TMT) and Triethyltin (TET) stimulated the spontaneous release of [3H]noradrenaline ([3H]NA) from hippocampal slices in a time- and concentration-dependent manner. TMT was the most potent compound, exhibiting an EC50 value 10-fold lower (3.8 μM) than that of TET (39.5 μM). Metal-evoked [3H]NA release did not increase in the absence of desipramine and was completely blocked by reserpine preincubation, indicating a vesicular origin of [3H]NA release but not a mechanism involving reversal of the transmitter transporter. The voltage-gated Na+ channel blocker tetrodotoxin (TTX) did not affect metal-evoked [3H]NA release. [3H]NA release elicited by TMT was partially extracellular Ca2+-dependent, since it was significantly decreased in a Ca2+-free EGTA-containing medium, whereas TET induced an extracellular Ca2+-independent release of [3H]NA. Neither inhibitors of Ca2+-entry through Na+/Ca2+exchanger and voltage-gated calcium channels, nor agents that interfere with Ca2+-mobilization from intracellular stores affected [3H]NA release induced by TMT. TET-evoked [3H]NA release was reduced by ruthenium red, which depletes mitochondrial Ca2+stores, but was not modified by caffeine and thapsigargin, which interfere with Ca2+mobilization from endoplasmic reticulum. The fact that TET effect was also attenuated by DIDS, an inhibitor of anion exchange, indicates that the effect of TET on spontaneous [3H]NA release may be mediated by intracellular mobilization of Ca2+ from mitochondrial stores through a Cl− dependent mechanism.

Coral Sanfeliu - One of the best experts on this subject based on the ideXlab platform.

  • neurotoxic effects of trimethyltin and Triethyltin on human fetal neuron and astrocyte cultures a comparative study with rat neuronal cultures and human cell lines
    Toxicology Letters, 2004
    Co-Authors: Rosa Cristofol, Sergi Gasso, David Vilchez, Maria Pertusa, E Rodriguezfarre, Coral Sanfeliu
    Abstract:

    Abstract Trimethyltin (TMT) and Triethyltin (TET) caused cell death in cultures of primary human neurons and astrocytes, rat neurons and human neuroblastoma cell lines. Human neurons and astrocytes showed a delayed response to TMT cytotoxicity. After 24 h of TMT exposure, LC50 values were 148.1, 335.5 and 609.7 μM for SK-N-MC neuroblastoma cell line, neurons and astrocytes, respectively. Over 5 days of exposure, the cytotoxic potency of TMT increased about 70-fold in human cortical neurons. Rat hippocampal neurons were the most vulnerable cells to TMT cytotoxicity, exhibiting an LC50 value 30-fold lower (1.4 μM) than that of rat cerebellar granule cells (44.28 μM). With the exception of rat hippocampal neurons, TET was more potent than TMT in inducing cell death (LC50 values of 3.5–16.9 μM). Moreover, TET was more effective than TMT in increasing intracellular free Ca2+ concentration in human and rat neurons. This work shows that human fetal neuron and astrocyte cultures are a useful model for studying the neurotoxic effects of these environmental contaminants and, thus, predicting their impact on human health.

  • trimethyltin and Triethyltin differentially induce spontaneous noradrenaline release from rat hippocampal slices
    Toxicology and Applied Pharmacology, 2000
    Co-Authors: Sergi Gasso, E Rodriguezfarre, Coral Sanfeliu, Cristina Sunol, Rosa Cristofol
    Abstract:

    The environmental contaminants trimethyltin (TMT) and Triethyltin (TET) stimulated the spontaneous release of [3H]noradrenaline ([3H]NA) from hippocampal slices in a time- and concentration-dependent manner. TMT was the most potent compound, exhibiting an EC50 value 10-fold lower (3.8 μM) than that of TET (39.5 μM). Metal-evoked [3H]NA release did not increase in the absence of desipramine and was completely blocked by reserpine preincubation, indicating a vesicular origin of [3H]NA release but not a mechanism involving reversal of the transmitter transporter. The voltage-gated Na+ channel blocker tetrodotoxin (TTX) did not affect metal-evoked [3H]NA release. [3H]NA release elicited by TMT was partially extracellular Ca2+-dependent, since it was significantly decreased in a Ca2+-free EGTA-containing medium, whereas TET induced an extracellular Ca2+-independent release of [3H]NA. Neither inhibitors of Ca2+-entry through Na+/Ca2+exchanger and voltage-gated calcium channels, nor agents that interfere with Ca2+-mobilization from intracellular stores affected [3H]NA release induced by TMT. TET-evoked [3H]NA release was reduced by ruthenium red, which depletes mitochondrial Ca2+stores, but was not modified by caffeine and thapsigargin, which interfere with Ca2+mobilization from endoplasmic reticulum. The fact that TET effect was also attenuated by DIDS, an inhibitor of anion exchange, indicates that the effect of TET on spontaneous [3H]NA release may be mediated by intracellular mobilization of Ca2+ from mitochondrial stores through a Cl− dependent mechanism.