Hdl Handle:
http://hdl.handle.net/10675.2/57
Title:
Lectin-based food poisoning: a new mechanism of protein toxicity.
Authors:
Miyake, Katsuya; Tanaka, Toru; McNeil, Paul L.
Abstract:
BACKGROUND: Ingestion of the lectins present in certain improperly cooked vegetables can result in acute GI tract distress, but the mechanism of toxicity is unknown. In vivo, gut epithelial cells are constantly exposed to mechanical and other stresses and consequently individual cells frequently experience plasma membrane disruptions. Repair of these cell surface disruptions allows the wounded cell to survive: failure results in necrotic cell death. Plasma membrane repair is mediated, in part, by an exocytotic event that adds a patch of internal membrane to the defect site. Lectins are known to inhibit exocytosis. We therefore tested the novel hypothesis that lectin toxicity is due to an inhibitory effect on plasma membrane repair. METHODS AND FINDINGS: Repair of plasma membrane disruptions and exocytosis of mucus was assessed after treatment of cultured cell models and excised segments of the GI tract with lectins. Plasma membrane disruptions were produced by focal irradiation of individual cells, using a microscope-based laser, or by mechanical abrasion of multiple cells, using a syringe needle. Repair was then assessed by monitoring the cytosolic penetration of dyes incapable of crossing the intact plasma membrane. We found that cell surface-bound lectins potently inhibited plasma membrane repair, and the exocytosis of mucus that normally accompanies the repair response. CONCLUSIONS: Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning.
Citation:
PLoS ONE. 2007 Aug 1; 2(8):e687
Issue Date:
1-Aug-2007
URI:
http://hdl.handle.net/10675.2/57
DOI:
10.1371/journal.pone.0000687
PubMed ID:
17668065
PubMed Central ID:
PMC1933252
Type:
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
ISSN:
1932-6203
Appears in Collections:
Institute of Molecular Medicine and Genetics: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorMiyake, Katsuyaen_US
dc.contributor.authorTanaka, Toruen_US
dc.contributor.authorMcNeil, Paul L.en_US
dc.date.accessioned2010-09-24T21:26:49Z-
dc.date.available2010-09-24T21:26:49Z-
dc.date.issued2007-08-01en_US
dc.identifier.citationPLoS ONE. 2007 Aug 1; 2(8):e687en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid17668065en_US
dc.identifier.doi10.1371/journal.pone.0000687en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/57-
dc.description.abstractBACKGROUND: Ingestion of the lectins present in certain improperly cooked vegetables can result in acute GI tract distress, but the mechanism of toxicity is unknown. In vivo, gut epithelial cells are constantly exposed to mechanical and other stresses and consequently individual cells frequently experience plasma membrane disruptions. Repair of these cell surface disruptions allows the wounded cell to survive: failure results in necrotic cell death. Plasma membrane repair is mediated, in part, by an exocytotic event that adds a patch of internal membrane to the defect site. Lectins are known to inhibit exocytosis. We therefore tested the novel hypothesis that lectin toxicity is due to an inhibitory effect on plasma membrane repair. METHODS AND FINDINGS: Repair of plasma membrane disruptions and exocytosis of mucus was assessed after treatment of cultured cell models and excised segments of the GI tract with lectins. Plasma membrane disruptions were produced by focal irradiation of individual cells, using a microscope-based laser, or by mechanical abrasion of multiple cells, using a syringe needle. Repair was then assessed by monitoring the cytosolic penetration of dyes incapable of crossing the intact plasma membrane. We found that cell surface-bound lectins potently inhibited plasma membrane repair, and the exocytosis of mucus that normally accompanies the repair response. CONCLUSIONS: Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Membrane / drug effects / metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEpithelial Cells / cytology / drug effectsen_US
dc.subject.meshExocytosis / physiologyen_US
dc.subject.meshFluorescent Dyes / metabolismen_US
dc.subject.meshFoodborne Diseases / etiologyen_US
dc.subject.meshGastric Mucosa / cytology / drug effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshLasersen_US
dc.subject.meshMucus / secretionen_US
dc.subject.meshPlant Lectins / toxicityen_US
dc.subject.meshRatsen_US
dc.titleLectin-based food poisoning: a new mechanism of protein toxicity.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, U.S. Gov't, Non-P.H.S.en_US
dc.identifier.pmcidPMC1933252en_US
dc.contributor.corporatenameInstitute of Molecular Medicine and Geneticsen_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomyen_US

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