Scheme summarizing the main results in this work.

<p>Etomoxir decreases respiration while increasing glycolytic activity. In addition, it causes oxidative stress (ROS over-production, GSH depletion) which, together with AMPK activation, may explain the potentiation of ATO-provoked apoptosis. Etomoxir may also cooperate in some cell models with glycolytic inhibitors (2-DG, lonidamine) to cause apoptosis. This response is further enhanced by co-incubation with ATO, due to the capacity of this agent to attenuate the 2-DG/etomoxir-provoked Akt and ERK activation.