Traumatic versus postischemic induction of oxidative stress in rat liver

A series of experiments was performed to characterize the effects of tissue trauma, extracellular calcium concentration, and prior ischemia on oxidative stress, measured by the accumulation of malondialdehyde-like materials (MDA-LM) in slices of rat liver. Liver tissue was rendered ischemic for 1 hour at 37 degrees C, either minced (to create traumatized fragments) or cleanly cut and washed (to create nontraumatized fragments), and then reoxygenated for 30 minutes in flasks of buffered salt solution. Nonischemic tissue was incubated similarly but without the 60-minute prior ischemia. The production of MDA-LM in the tissues was used as an indicator of lipid peroxidation. Production of MDA-LM in the tissues was used as an indicator of lipid peroxidation. Production of MDA-LM was always enhanced by prior ischemia and reoxygenation. However, trauma also increased the production of MDA-LM both in nonischemic liver slices in vitro and in those subjected to ischemia and reoxygenation. Furthermore, the elimination of calcium from incubation buffer significantly reduced MDA-LM production both in nontraumatized, ischemic, and reoxygenated tissues and in traumatized, nonischemic tissues; while the addition of the calcium ionophore A23187 (10 mumol/L) increased MDA-LM production in nontraumatized tissues independently of ischemia and reoxygenation. In nonischemic, traumatized tissues, the iron chelators deferoxamine and CGP-46,700A (1,2-diethyl-3-hydroxypyrid-4-one) quenched MDA-LM production. These data indicate that either ischemia or mechanical trauma may predispose liver tissue to calcium-dependent and iron-dependent oxidative stress.