ADDITIONAL EVIDENCE OF AUTOXIDATION AS A POSSIBLE MECHANISM OF NEUTROPHIL LOCOMOTORY DYSFUNCTION IN BLUNT TRAUMA

Previous studies in victims of blunt injury suggest that the observed neutrophil (PMN) locomotory dysfunction is, in part, due to autoxidation. To further clarify the occurrence and significance of autoxidation, we studied changes in levels of glutathione in PMN and of ascorbic acid and α-tocopherol in serum and blood cells of postsurgical and blunt trauma patients. Levels of total, reduced, and oxidized glutathione in PMN from trauma patients were similar to normal controls. Serum and cellular ascorbic acid and α-tocopherol levels dropped significantly after injury and remained below normal control levels during the 7 to 8-day study period. Low serum α-tocopherol was partially explainable on the basis of changes in serum lipids. When serum samples of trauma patients were thawed unprotected without pyrogallol, there was significant loss of recoverable α-tocopherol, whereas no significant losses occurred with unprotected thawed normal sera. Less total reducing capacity was observed in PMN of trauma patients compared with normal controls. These findings indicate that synthesis and regeneration capacity of glutathione are intact but that the levels of the consumable antioxidants, ascorbic acid, and α-tocopherol are compromised after injury. These results add further support to the hypothesis that autoxidation occurs in trauma.