In experiments to test this hypothesis, the team showed that intestinal mucin stops the degradation of cells caused by exposure to copper, but it still allows copper-starved cells to safely take in copper ions and recover. The researchers conducted their experiments in laboratory dishes, but they believe the processes they revealed are the same as those that take place in the body, says Reznik.
The study’s findings suggest that intestinal mucin is a chaperone, a sort of assistant protein, for copper. Thanks to its two copper-binding sites, mucin ensures the proper behavior of this sometimes troublemaking metal. The researchers think the mucin chaperone might also be involved in delivering copper to the microbes in our gut, which also need this trace metal.
“It’s been well-known for decades that copper is chaperoned by proteins inside cells, but nobody thought to ask what happens to copper when you first ingest it,” Fass says.
No loose electrons get by the mucin chaperone
The study suggests that intestinal mucin might also prevent the squandering of antioxidants – beneficial molecules that have electrons to spare – by stopping electrons from flowing continuously from antioxidants to copper to oxygen. By holding on to single-charged copper ions, mucin seems to prevent this cycle.
Says Fass: “For example, what happens if you eat a copper-rich meal and drink orange juice, which contains vitamin C, an antioxidant? How do you prevent a flow of electrons from vitamin C and the resulting generation of reactive oxygen? Apparently, by holding on to single-charged copper ions at dedicated binding sites, the intestinal mucin blocks this flow.”