The effect of quinacrine on oxidative stress in kidney tissue stored at low temperature after warm ischemic injury.

Rabbit kidney cortex tissue slices were made ischemic (37 degrees C) for 60 min and then either reperfused in warm (37 degrees C) oxygenated physiologic buffer for 210 min or placed in UW Na gluconate solution (+/- quinacrine; 100 micromol/L) for 18 h followed by warm aerobic reperfusion. Slices were sampled at intervals and analyzed for malondialdehyde (MDA) content by HPLC. Control (nonischemic) slices had no change in MDA content over the duration of the experiment. Hypothermic storage of nonischemic slices did not result in any increase in MDA during reperfusion. Ischemic slices showed significant increases in MDA content during the first 1.5 h of reperfusion and remained elevated for the remainder of the experiment. Hypothermic storage of warm ischemic kidney slices resulted in a significant decrease in MDA content during the storage period. However, MDA content in these slices increased during warm reperfusion and was significantly higher than that in nonischemic controls. Quinacrine added during hypothermic storage of warm ischemic slices significantly decreased slice MDA content during warm reperfusion, an effect which was lost by increasing the storage solution calcium content. This study shows that aerobic hypothermic storage can aid in reducing oxidative stress in warm ischemic kidney tissue during reperfusion. This study suggests that the effects of quinacrine are at the level of the mitochondrion and not as an antioxidant compound.