Differences in glycolytic capacity and hypoxia tolerance between hepatoma cells and hepatocytes

✍ Scribed by Doris Hugo-Wissemann; Irene Anundi; Werner Lauchart; Richard Viebahn; Dr. Herbert de Groot

• Book ID: 102850792
• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 704 KB
• Volume: 13
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840130215

✦ Synopsis

D-7400 Tubingen, Federal Republic of Germany

Viability, glycolytic capacity and energy metabolism under anaerobic conditions were studied in the hepatoma cell lines HTC, FU5 and HepG2 and in rat and human hepatocytes using glucose and fructose as glycolytic precursors. During 6 hr of anaerobic incubation without additional substrate, viability decreased rapidly in FUS and HTC cells, whereas viability of HepG2 cells was not significantly affected. In all tumor cells, 10 mmol/L glucose prevented hypoxic cell injury almost completely. Lactate formation from glucose was about five times higher than in hepatocytes under these circumstances. ATP content of the tumor cells remained almost constant under anaerobic conditions in the presence of glucose. Ten millimoles per liter of fructose diminished glycolysis in the hepatoma cells compared with glucose, ranging from 87% reduction in HTC cells to 43% reduction in HepGt cells. Accordingly, ATP content decreased rapidly in the FU5 and slowly in the HepG2 cells. Viability was strongly diminished in the HTC and FU5 cells in the presence of fructose, whereas in the HepG2 cells no effect of fructose on viability was detectable. In contrast to the hepatoma cells, rat and human hepatocytes exhibited higher rates of anaerobic glycolysis in the presence of fructose and thus were able to maintain their viability under these conditions. These differences in glycolytic capacity, energy metabolism and hypoxia tolerance of hepatoma cells compared with hepatocytes may be used for the treatment of liver cancer by isolated liver perfusion andex situ revision of the organ. (H EPATOLOGY 1991; 13~297-303.) Carcinogenesis involves complex changes in the patterns of enzyme activities (1-4). Enzymes typical for a specialized organ such as the liver are replaced by unspecific enzymes of fetal or muscle type (5). The