Abstract:
The increase prevalence of obesity in the population has led to more flexible criteria for accepting liver allograft in hepatic transplant, while steatosis is an established risk factor for postoperative complications. Hypothermic storage of livers prior to transplantation is generally used to preserve liver allografts. However, injury to allografts during ischemia/reperfusion is inevitable. Therefore there is a need to develop strategies aiming at increasing the organ pool. Steatotic liver diseases might implicate in mitochondrial dysfunction associated with elevated free radical damages. The aim was to assess mitochondrial respiration and reactive oxygen species (ROS) simultaneously at 37°C and 7°C on a model system of isolated perfused lean Zucker and diabetic fatty rat livers by using the Oxygraph-2 K that connected to a house-built fluro-spectrometer. The result showed cold temperature depressed mitochondrial oxygen fluxes. However there was no significant difference in mitochondrial respiratory capacities between both groups of livers at 7°C and 37°C in which was consistent with similar mitochondrial mass maker (citrate synthase) found in both groups. Decreased temperature however remarkably increased ROS leakage in both groups. Moreover, increase in Complex Iinduced ROS production seemed to associate with Complex I dysfunction in steatotic livers. A marginal increase of lactate dehydrogenase activities in steatotic livers appeared to have the power over the liver‘s buffering capacity in which could lead to cellular pH changes and thus decrease cell viability. These findings indicated that hypothermia did induce metabolic depression but did not decrease ROS production in both lean and steatotic livers. Moreover, steatotic livers appeared to be vulnerable to cold ischemia/reperfusion injury.
