Antioxidants prevent the cellular deficit produced in response to burn injury

We studied the effect of water-soluble antioxidants on the cell energetics in multiple organs in rats in response to a 20% total body surface area third-degree burn injury. Liver, lung, and heart tissue were studied. Cell energetics were measured as tissue energy charge potential (ECP), adenosine triphosphate (ATP) content, and total adenine nucleotides. The enzymatic antioxidant catalase was used as a marker of endogenous cell antioxidant activity, especially to hydrogen peroxide. The water-soluble antioxidants glutathione, N-acetylcysteine, and vitamin C were given orally beginning at the time of burn injury and for the 6-day study period. All rats were fluid resuscitated according to the Parkland formula. The mortality rate was 0% for this size burn. The ECP in lung, liver, and heart, was normal on day 1 after the burn injury. However, the ECP was significantly decreased from the controls in the liver by day 3, with a peak decrease at day 6 as inflammation increased. A decrease in the heart ECP occurred between day 3 and day 6. Total adenine nucleotides did not decrease, indicating the decrease in ECP to be the result of a decrease in ATP. ECP remained normal in the lung. Catalase was also decreased in the liver and the heart and remained at normal levels in the lung. The decrease in the liver and heart ECP and ATP was eliminated with the oral antioxidant administration after the burn injury. We conclude that a modest burn injury decreases cellular energy charge in the heart and liver not immediately after burn but 3 to 6 days later. The decrease in antioxidant activity precedes the decrease in ECP. The lung appears to be protected. Water-soluble antioxidants, given after burn injury, prevent the altered cell energetics-strongly suggesting a cause-and-effect relationship between increased oxidant release with inflammation, decreased antioxidant activity, and altered cell energetics.