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A clearly recognized function of GSTs is their participation in antioxidative reactions together with the pivotal cellular antioxidant GSH in order to eliminate ROS and lipid hydroperoxides that accumulate in infected tissues (Figure 1) (Wagner et al., 2002)

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

Supervised care is not a marketing claim

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Coli cytosine deaminase (CD) gene

The presence of risk factors for overdose should not prevent the management of pain in any patient (see WARNINGS