Protective effect of fructose on survival and metabolic capacities of hepatocytes kept overnight under cold hypoxia before normothermic reoxygenation.

The protective effect of fructose with regard to hypoxia-induced cell injury in overnight cold preserved hepatocytes (20 hr at 4 degrees C) was investigated. The addition of fructose (at 10 and 20 mM) resulted in an improved survival of hepatocytes during their normothermic (37 degrees C) reoxygenation, irrespective of the time of fructose addition before the onset of hypoxia (i.e. 10, 20 or 30 min). Such a protective effect was even higher than that observed when hepatocytes were incubated in the University of Wisconsin solution (UW). Moreover, neither Desferal (an iron chelator) nor adenosine (an ATP precursor), nor other carbohydrates (glucose, galactose and the antioxidant mannitol) were able to protect cells against such an hypoxia-mediated injury. The intracellular ATP content was lower in both adenosine- and fructose-treated hepatocytes than in control untreated cells. However, the cellular metabolic capacities such as protein synthesis and gluconeogenesis from lactate recovered faster during reoxygenation of previously hypoxic fructose-treated cells compared with both control and adenosine-treated cells.