A skin burn produces a decrease in cell energy charge potential (ECP), a marker of cell function, in the liver and other organs. The process appears to be oxidant induced because reduced glutathione (GSH) appears to be protective. The gut mucosal barrier is also known to be altered after burns and appears to be improved by glutamine, which is a source of energy and GSH production. Neither the relationship between the gut barrier change and the ECP of the gut barrier nor the mechanism of glutamine protection has been defined. The effect of a 20% total body surface area, full-thickness burn in a rat on ECP and GSH content in the ileum and the liver and the effect of oral glutamine (1 g/kg/d) on any changes were studied. Three groups of rats (14 rats per group) were studied: a control group, a group with burns alone, and a group with burns that were given glutamine. Half of the rats were killed 1 day after the burn, and the other half were killed 6 days after the burn. ECP did not decrease 1 day after the burn, but 6 days after the burn, ECP decreased from a control of 0.53+/-0.06 to 0.41+/-0.01 in the liver and from 0.64+/-0.04 to 0.29+/-0.04 in the ileum. In the ileum, glutamine prevented the decrease of the ECP (which increased to 0.58+/-.03), but in the liver, glutamine did not alter the ECP (which remained at 0.42+/-0.05). The GSH content was unchanged after the burn injury in both organs compared with the value before the burn injury. It can be concluded that a delayed decrease in ECP in the ileum occurs after a burn injury. Orally administered glutamine prevents the decrease in ECP, probably by providing cell energy rather than by increasing gut GSH (antioxidant) activity.