Some 1 million people in the United States suffer from inflammatory bowel disease. In the colon, this disease is called ulcerative colitis; in the small intestine, it’s Crohn’s disease. Though physicians know little about what causes these conditions, each results in abdominal pain and debilitating, bloody diarrhea. Now, researchers have uncovered evidence that the conditions may initially be triggered by chemical reactions that deplete affected tissues of a key antioxidant.
Matthew B. Grisham and Tak Yee Aw of Louisiana State University Health Science Center in Shreveport have been working with mice genetically engineered to spontaneously develop the disease. They recently noticed that 5 weeks before occurrence of the hallmark intestinal inflammation, concentrations of one antioxidant–reduced glutathione–begin falling in the animal’s gut. By the time inflammation appeared, this antioxidant had dropped by 80 percent in affected gut tissue.
To confirm the role of oxidative reactions in the gut, Grisham and Aw added a potent antioxidant, n-acetyl cysteine, to the sick animals’ drinking water. In short order, glutathione concentrations rose to nearly normal levels and inflammation in the rodents’ guts decreased significantly.
Grisham notes that some genes respond to cellular oxidation by revving up the immune system, thereby triggering inflammation. He says his new findings hint that patients may one day be able to better tame the runaway inflammation of inflammatory bowel disease by using antioxidant therapies.