@article{Leist1996novel-7152,
  year={1996},
  doi={10.1016/S0168-8278(96)80301-1},
  title={A novel mechanism of murine hepatocyte death inducible by Concanavalin A},
  number={6},
  volume={25},
  issn={0168-8278},
  journal={Journal of Hepatology},
  pages={948--959},
  author={Leist, Marcel and Wendel, Albrecht}
}

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    <dcterms:title>A novel mechanism of murine hepatocyte death inducible by Concanavalin A</dcterms:title>
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    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:32:15Z</dc:date>
    <dc:creator>Leist, Marcel</dc:creator>
    <dcterms:abstract xml:lang="eng">Background: Concanavalin A (Con A) is a plant lectin that polyclonally activates T-cells. When given intravenously to mice it induces a selective liver failure. Hepatotoxicity following Con A administration involves the systemic release of tumor necrosis factor.&lt;br /&gt;Methods: We used primary murine hepatocyte cultures to investigate mechanisms of hepatocytotoxicity related to this animal model of inflammatory liver failure.&lt;br /&gt;Results: Con A was directly toxic for cultured hepatocytes. This toxicity did not require additional cytokines or the presence of T cells. Cytotoxicity due to Con A involved specific binding of the lectin to mannosyl cell surface receptors, but no internalization. Other structurally similar lectins lacked such an in vitro hepatocytotoxicity. Con A induced initially reversible alterations of the morphology that were different from the ones caused by classical hepatotoxins. Con A-induced cell death was highly specific for murine hepatocytes. It was neither apoptotic by morphology nor did it involve DNA fragmentation. In addition, Con A caused a fall in cellular total glutathione content and an increase in transcriptional activity. Stabilization of microtubules by taxol completely protected cells from the lectin.&lt;br /&gt;Conclusions: Stimulation of hepatocytes with Con A elicits a novel mechanism of cytotoxicity due to inappropriate excessive stimulation of membrane receptors and subsequent disturbance of the cytoskeleton.</dcterms:abstract>
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    <dc:creator>Wendel, Albrecht</dc:creator>
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    <dcterms:bibliographicCitation>First publ. in: Journal of Hepatology 25 (1996), 6, pp. 948-959</dcterms:bibliographicCitation>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <dcterms:issued>1996</dcterms:issued>
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