Abstract.
Cancer cell metabolism is characterized by limited oxidative phosphorylation in order to minimize oxidative stress. We have previously shown that the flavonoid flavone in HT-29 colon cancer cells increases the uptake of pyruvate or lactate into mitochondria, which is followed by an increase in O−.2. production that finally leads to apoptosis. Similarly, a supply of palmitoylcarnitine in combination with carnitine induces apoptosis in HT-29 cells by increasing the mitochondrial respiration rate. Here we show that flavone-induced apoptosis is increased more than twofold in the presence of palmitoylcarnitine due to increased mitochondrial fatty acid transport and the subsequent metabolic generation of O−.2 in mitochondria is the initiating factor for the execution of apoptosis.
Key words. HT-29 human colon cancer cells, superoxide anion generation, mitochondrial apoptosis pathway, fatty acid transport.
Footnotes
Received 12 August 2005; received after revision 12 October 2005; accepted 14 October 2005