In vitro inhibitory effect of chitosan and its degradation products on energy metabolism in Ehrlich ascites tumour cells (EAT)

Abstract

Chitosan, a product of depolymerization and deacetylation of chitin, as polycation, diminishes glycolysis, i.e. aerobic lactate formation both, in Ehrlich ascites tumour (EAT) intact cells and in their cytosolic fraction. By inhibiting glycolysis, chitosan decreases also glucose uptake and ATP level in intact cells. Chitosan does not exert a similar inhibitory effect on glycolytic activity of mouse normal liver and muscle supernatants. It has been found that a decrease in glycolytic activity and cell ATP level in tumour cells is caused by inhibition of tumour specific variant of pyruvate kinase from fraction B (isoenzyme M2).