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Therefore, the major oxidative burst during I/R occurs after the reexposure to oxygen during the so called warm ischemia time.7 Although the molecular mechanisms involved in I/R cellular responses are still not fully understood, a major role seems to be played by APE/Ref-1 and NF-B proteins in liver.42 Overexpression of APE/Ref-1 by adenoviral vector resulted in suppression of the reperfusion-generated oxidative stress in a mouse model.42 Liver transplantation (LT) is at present the only available choice for the treatment of end-stage hepatic disease

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open arrowheads in 3a, 4a, and Supplementary Fig

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The container must be rigid, leak-resistant, puncture-resistant, with a tight screw cap, and clearly labeled (e.g., SHARPS DO NOT RECYCLE)