Katsuya Miyake/Josai University (Japan) and Paul McNeil/Medical College of Georgia

Bean lethal.
Healthy epithelial cells absorb a green dye (left), whereas cells exposed to lectins cease repairs and die, absorbing a red dye.

Red Bean Revenge

If undercooked, a veggie meal can wreak just as much havoc on your gastrointestinal (GI) tract as improperly prepared meat, fish, or dairy products. Now researchers think they know why, at least as far as legumes are concerned.

Many types of beans contain a class of proteins called lectins. Researchers have long known that, if not destroyed by cooking, lectins can cause a severe form of food poisoning with attendant nausea, vomiting, and diarrhea. But no one understood exactly how the molecules worked their mischief.

The key appears to be lectins' ability to shut down the cell membrane repair process that occurs as a part of digestion. That's what an international team of researchers observed when working with single cells and small specimens of mouse gut: Lectins bound to the membrane-repairing proteins of intestinal epithelial cells, effectively inactivating them. As a result, the cells began to die almost immediately, the team reports online this week in PLoS One. "It was the most dramatic inhibition of membrane repair that we had ever seen," says cellular biologist and co-author Paul McNeil of the Medical College of Georgia in Augusta.

Although the team hasn't directly observed the effect of lectins on the lower GI tracts of living animals, "there is no reason to think it would be different," says McNeil. Now that the researchers have found how lectins can cause food poisoning, he adds, they can begin studying the role of membrane-repair failure in other GI conditions such as Celiac disease and cancer.

The researchers have "made a connection nobody has made before" between lectins and cell-membrane repair, says cellular biologist Richard Steinhardt of the University of California, Berkeley. By linking a cellular biology phenomenon to a medical phenomenon, says Steinhardt, who acted as academic editor of the article for PLoS One, the researchers have produced findings that could indeed have implications for other studies of diseases that interfere with or destroy the membrane repair process.

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