Figure 1: Mechanism expressed doxorubicin-dependent free radical generation and reportedly proposed role of triiodothyronine in redox equilibrium. P450R and iNOS transfer one electron to doxorubicin (DOX) from NADPH2 leading to synthesis of doxorubicin radical (DOX*). Subsequently, electron is taken by O2 and to produce superoxide anion radical ( O 2 ). That is staring point to oxidative stress. Seemingly paradoxically NADPH2 is indispensable to antioxidative activity, and its synthesis is transcriptionally regulated by triiodothyronine (T3).