Proposed model of doxorubicin metabolism in ALL cells that emphasizes the toxicity-generating and signal-generating modules comprising the network.

The toxicity-generating module is NADPH-limited at the high Dox condition, allowing DHEA administration to decrease NADPH-dependent semiquinone doxorubicin formation. The signal-generating module is NADPH-limited at the low Dox condition, allowing DHEA administration to decrease NADPH-dependent superoxide formation.