Lectin-based food poisoning: a new mechanism of protein toxicity.
dc.contributor.author | Miyake, Katsuya | |
dc.contributor.author | Tanaka, Toru | |
dc.contributor.author | McNeil, Paul L. | |
dc.date.accessioned | 2010-09-24T21:26:49Z | |
dc.date.available | 2010-09-24T21:26:49Z | |
dc.date.issued | 2007-08-01 | en_US |
dc.identifier.citation | PLoS ONE. 2007 Aug 1; 2(8):e687 | en_US |
dc.identifier.issn | 1932-6203 | en_US |
dc.identifier.pmid | 17668065 | en_US |
dc.identifier.doi | 10.1371/journal.pone.0000687 | en_US |
dc.identifier.uri | http://hdl.handle.net/10675.2/57 | |
dc.description.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. | |
dc.rights | The 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.mesh | Animals | en_US |
dc.subject.mesh | Cell Membrane / drug effects / metabolism | en_US |
dc.subject.mesh | Cells, Cultured | en_US |
dc.subject.mesh | Epithelial Cells / cytology / drug effects | en_US |
dc.subject.mesh | Exocytosis / physiology | en_US |
dc.subject.mesh | Fluorescent Dyes / metabolism | en_US |
dc.subject.mesh | Foodborne Diseases / etiology | en_US |
dc.subject.mesh | Gastric Mucosa / cytology / drug effects | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Lasers | en_US |
dc.subject.mesh | Mucus / secretion | en_US |
dc.subject.mesh | Plant Lectins / toxicity | en_US |
dc.subject.mesh | Rats | en_US |
dc.title | Lectin-based food poisoning: a new mechanism of protein toxicity. | en_US |
dc.type | Journal Article | en_US |
dc.type | Research Support, U.S. Gov't, Non-P.H.S. | en_US |
dc.identifier.pmcid | PMC1933252 | en_US |
dc.contributor.corporatename | Institute of Molecular Medicine and Genetics | en_US |
dc.contributor.corporatename | Department of Cellular Biology and Anatomy | en_US |
refterms.dateFOA | 2019-04-09T21:11:56Z | |
html.description.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. |