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PLoS ONE:豆科植物使人中毒的关键蛋白-植物凝血素 如果煮得欠火候,一顿蔬菜大餐可能会像腐烂的肉、鱼或奶制品一样对你的胃肠(GI)系统造成巨大的危害。对于这种食物的“报复”,如今,研究人员认为他们已经找到了背后原因,至少对于人们关心的豆科植物而言是这样。许多种类的豆科植物都包含有一种蛋白质——植物凝血素。研究人员早就知道,如果不通过烹饪破坏这种蛋白质,植物凝血素会导致一类严重的食物中毒,同时伴随恶心、呕吐和腹泻。然而迄今为止,科学家一直没有搞清这种
生物谷 如果煮得欠火候,一顿蔬菜大餐可能会像腐烂的肉、鱼或奶制品一样对你的胃肠(GI)系统造成巨大的危害。对于这种食物的“报复”,如今,研究人员认为他们已经找到了背后原因,至少对于人们关心的豆科植物而言是这样。
许多种类的豆科植物都包含有一种蛋白质——植物凝血素。研究人员早就知道,如果不通过烹饪破坏这种蛋白质,植物凝血素会导致一类严重的食物中毒,同时伴随恶心、呕吐和腹泻。然而迄今为止,科学家一直没有搞清这种分子使人中毒的确切机制。
问题的关键可能在于植物凝血素具有终止细胞膜修复过程——它是消化作用的一部分——的能力。这是一个国际研究小组通过对单细胞以及小鼠内脏少量标本进行观察后得出的结论——植物凝血素能够限制肠内上皮细胞的膜修复蛋白质的活动,有效地抑制其活性。在此前提下,细胞将会迅速消亡。研究小组在最新的《公共科学图书馆·综合》(PLoS ONE)杂志网络版上报告了这一研究成果。参与该项研究的美国奥古斯塔市佐治亚医学院的细胞生物学家Paul McNeil认为:“这是我们之前从未见过的最具戏剧性的膜修复抑制机制。”
McNeil表示,尽管研究小组并没有直接观察到植物凝血素对动物活体下层GI系统构成的影响,“但没有理由怀疑它们之间存在什么差别”。他强调,如今,研究人员已经找到了植物凝血素导致食物中毒的原因,他们将继续研究膜修复失效在其他GI疾病——例如腹腔疾病和癌症——中扮演的角色。
加利福尼亚大学伯克利分校的细胞生物学家Richard Steinhardt指出,研究人员在之前没有人关注的植物血凝素与细胞膜修复过程之间建立了联系。Steinhardt是《公共科学图书馆·综合》杂志的学术文章编辑。Steinhardt说,通过在一个细胞生物学现象与一个医学现象之间架设桥梁,研究人员的这一发现实际上对于其他干涉或破坏膜修复过程的疾病的研究具有借鉴意义。(科学时报)
原始出处:
PLoS one
Received: May 4, 2007; Accepted: June 25, 2007; Published: August 1, 2007
Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity
Katsuya Miyake1, Toru Tanaka2, Paul L. McNeil1,3*
1 Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Georgia, United States of America, 2 Faculty of Pharmaceutical Sciences, Josai University, Sakado, Saitama, Japan, 3 Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia, United States of America
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.
全文链接:
http://www.plosone.org/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0000687 |
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