In a previous investigation we demonstrated that reperfusion with a melatonin-containing medium enhanced bile production and tissue ATP levels in rat livers cold-preserved with University of Wisconsin (UW) or Celsior solutions respect to melatonin-free reperfusion; lipid peroxidation products in the perfusate were not influenced by the indole. This was ascribed to an increased efficiency of hepatocyte mitochondria induced by melatonin. Reactive oxygen species (ROS) normally leak from the electron transfer chain in mitochondria and excessive ROS production is presumed to mediate ischemia-reperfusion (I/R) damage. We used a histochemical reaction to demonstrate ROS on the same model. Respect to the lobular zonation of ROS in control livers, the stained area of cold-preserved livers reperfused without melatonin was restricted to a narrow portal region, in keeping with the much lesser ATP content. When reperfusion was made with melatonin liver morphology was improved and the ROS reaction in hepatocytes more intense, though not reaching the control liver pattern. Sinusoidal cells were poorly stained in both cases. In conclusion, with this different approach we confirmed that melatonin improved mitochondria performance and discriminated parenchymal from sinusoidal cell behavior. Our observations confirm that melatonin mitigates I/R injury and support its potential in liver transplantation.
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