生物谷 如果煮得欠火候,，一頓蔬菜大餐可能會(huì)像腐爛的肉,、魚或奶制品一樣對(duì)你的胃腸（GI）系統(tǒng)造成巨大的危害。對(duì)于這種食物的“報(bào)復(fù)”,，如今,，研究人員認(rèn)為他們已經(jīng)找到了背后原因，至少對(duì)于人們關(guān)心的豆科植物而言是這樣,。
許多種類的豆科植物都包含有一種蛋白質(zhì)——植物凝血素,。研究人員早就知道，如果不通過(guò)烹飪破壞這種蛋白質(zhì),，植物凝血素會(huì)導(dǎo)致一類嚴(yán)重的食物中毒,，同時(shí)伴隨惡心,、嘔吐和腹瀉。然而迄今為止,，科學(xué)家一直沒(méi)有搞清這種分子使人中毒的確切機(jī)制,。
問(wèn)題的關(guān)鍵可能在于植物凝血素具有終止細(xì)胞膜修復(fù)過(guò)程——它是消化作用的一部分——的能力。這是一個(gè)國(guó)際研究小組通過(guò)對(duì)單細(xì)胞以及小鼠內(nèi)臟少量標(biāo)本進(jìn)行觀察后得出的結(jié)論——植物凝血素能夠限制腸內(nèi)上皮細(xì)胞的膜修復(fù)蛋白質(zhì)的活動(dòng),，有效地抑制其活性,。在此前提下，細(xì)胞將會(huì)迅速消亡,。研究小組在最新的《公共科學(xué)圖書館·綜合》（PLoS ONE）雜志網(wǎng)絡(luò)版上報(bào)告了這一研究成果,。參與該項(xiàng)研究的美國(guó)奧古斯塔市佐治亞醫(yī)學(xué)院的細(xì)胞生物學(xué)家Paul McNeil認(rèn)為：“這是我們之前從未見(jiàn)過(guò)的最具戲劇性的膜修復(fù)抑制機(jī)制。”
McNeil表示,，盡管研究小組并沒(méi)有直接觀察到植物凝血素對(duì)動(dòng)物活體下層GI系統(tǒng)構(gòu)成的影響,，“但沒(méi)有理由懷疑它們之間存在什么差別”。他強(qiáng)調(diào),，如今,，研究人員已經(jīng)找到了植物凝血素導(dǎo)致食物中毒的原因，他們將繼續(xù)研究膜修復(fù)失效在其他GI疾病——例如腹腔疾病和癌癥——中扮演的角色,。
加利福尼亞大學(xué)伯克利分校的細(xì)胞生物學(xué)家Richard Steinhardt指出,，研究人員在之前沒(méi)有人關(guān)注的植物血凝素與細(xì)胞膜修復(fù)過(guò)程之間建立了聯(lián)系。Steinhardt是《公共科學(xué)圖書館·綜合》雜志的學(xué)術(shù)文章編輯,。Steinhardt說(shuō),，通過(guò)在一個(gè)細(xì)胞生物學(xué)現(xiàn)象與一個(gè)醫(yī)學(xué)現(xiàn)象之間架設(shè)橋梁，研究人員的這一發(fā)現(xiàn)實(shí)際上對(duì)于其他干涉或破壞膜修復(fù)過(guò)程的疾病的研究具有借鑒意義,。（科學(xué)時(shí)報(bào)）
原始出處:
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.
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