Research: Lipid Peroxidation Following Thermal Injury

Abstract

Formation of lipid peroxides in vivo leads to a variety of normal and pathologic consequences. For instance, peroxidation of cell membrane lipids results in altered membrane properties and increased cell destruction. Following severe thermal injury, elevated plasma levels of malondialdehyde, one product of lipid peroxidation, were detected, which suggests that an elevated level of lipid peroxidation was occurring in those patients. In vivo the major mechanisms to protect cells from lipid peroxidation are the presence of vitamin E, the fat-soluble antioxidant, and destruction of peroxides by glutathione peroxidase. In four of five patients investigated, the plasma content of vitamin E was low. The erythrocyte glutathione peroxidase activity was initially low in two patients and, by 15 days postburn, was below normal values in the other three patients. The results suggest that lipid peroxidation was occurring at elevated levels in these severely burned patients. An increased rate of lipid peroxidation could contribute to the decreased levels of phosphatidylethanolamine and essential polyunsaturated fatly acids in plasma and erythrocyte lipids and the shortened erythrocyte lifetimes previously observed in severely burned patients.