Hepatocyte anoxic injury is prevented by high concentration of fructose.

H UMAN livers can only be stored for a short time before transplantation, thus a better understanding of poteatial phannacologic and nutritional strategies that might protect the liver against anoxic damage may be imponant clinically. Fructose has been shown recently to prevent liver damage induced by Watnl ischemia as assessed by lactate dehydrogenase (LDH) release. I To determine whether fructose protects the liver from anoxic damage by production of glycolytic adenosine triphosphate tATP), and whether an elevation of cytosolic free calcium (Ca/+) is involved in anoxic liver cell injury, the intracetiular A TP level in real time assessed by 31p nuclear magnetic resonance (NMR) spectroscopy and intracellular free calcium determinations with aequorin using freshly isolated rat hepatocytes was studied. Lactate dehydrogenase release was measured to monitor liver cell damage.