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Short-term caloric restriction induced bone loss in both axial and appendicular bones by increasing adiponectin

After the model was expanded to include GS-H 2 Q adduct formation as a function of its reduction potential, it was then combined with the Reed glutathione model 21 in order to simulate how the quinone redox-metabolism of doxorubicin influenced the glutathione metabolism

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Another important mechanism of oxidative stress-mediated damage is disturbed redox signalling

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