Intensification of Doxorubicin-Related Oxidative Stress in the Heart by Hypothyroidism Is Not Related to the Expression of Cytochrome P450 NADPH-Reductase and Inducible Nitric Oxide Synthase, As Well As Activity of Xanthine Oxidase

<table>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 NADPH<sub>2</sub> leading to synthesis of doxorubicin radical (DOX*).  Subsequently, electron is taken by O<sub>2</sub> and to produce superoxide anion radical (<svg height="15.65" id="M3" style="vertical-align:-3.13504pt" version="1.1" viewbox="0 0 31.3375 15.65" width="31.3375" xmlns="http://www.w3.org/2000/svg">
<g transform="matrix(1.25,0,0,-1.25,0,15.65)">
<g transform="translate(72,-59.48)">
<text transform="matrix(1,0,0,-1,-71.95,62.66)">
<tspan style="font-size: 12.50px; " x="0" y="0">O</tspan>
</text>
<text transform="matrix(1,0,0,-1,-62.92,59.53)">
<tspan style="font-size: 8.75px; " x="0" y="0">2</tspan>
<tspan style="font-size: 8.75px; " x="4.8699999" y="-8.3000002">−</tspan>
<tspan style="font-size: 8.75px; " x="10.86512" y="-8.3000002">∗</tspan>
</text>
</g>
</g>
</svg>). That is staring point to oxidative stress. Seemingly paradoxically NADPH<sub>2</sub> is indispensable to antioxidative activity, and its synthesis is transcriptionally regulated by triiodothyronine (T3). </table>

Oxidative Medicine and Cellular Longevity

fig1

Figure 1

Figure 1: Intensification of Doxorubicin-Related Oxidative Stress in the Heart by Hypothyroidism Is Not Related to the Expression of Cytochrome P450 NADPH-Reductase and Inducible Nitric Oxide Synthase, As Well As Activity of Xanthine Oxidase 

Figure 1 | Intensification of Doxorubicin-Related Oxidative Stress in the Heart by Hypothyroidism Is Not Related to the Expression of Cytochrome P450 NADPH-Reductase and Inducible Nitric Oxide Synthase, As Well As Activity of Xanthine Oxidase 