Cutaneous thermal burn and oxidant-mediated acute lung injury: Appearance in serum of lung-related LDH isoenzyme

Previous studies from our laboratory have demonstrated that thermal injury to the skin of rats is associated with the production of oxygen radicals by complement-activated blood neutrophils, resulting in acute lung injury as demonstrated by increases in lung vascular permeability and morphological evidence of vascular endothelial cell damage, interstitial edema, and alveolar hemorrhage. In the present study, the analysis of sera from thermally injured rats reveals an isoenzyme profile for lactate dehydrogenase (LDH;EC 1.1.1.27) that is compatible with origin from lung. The appearance of LDH-4 isoenzyme in serum of thermally injured rats correlates linearly with indices of lung damage, supporting the results of previous studies suggesting that thermal trauma to the skin can cause oxygen radical production by complement-activated blood neutrophils with resultant acute microvascular injury in the lung interstitium. Furthermore, interventions that protect from oxidant-mediated lung injury (catase, scavengers of hydroxyl radical, iron chelators or neutrophil depletion) result in significant reductions in serum levels of the LDH-4 isoenzyme following thermal injury to the skin. Thus, measurements of LDH isoenzyme patterns in serum to be useful in monitoring tissue damage such as oxygen radical-mediated acute lung injury.