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Figure 4 Alterations in the intracellular redox status are often associated with GSH depletion (Polonikov, 2020) and endogenous GSH deficiency, due either to decreased biosynthesis and/or increased consumption, is a marked contributor to the pathogenesis of numerous diseases via mechanisms including oxidative stress and inflammation
Such alterations may result from the increased NTBI that can be catalyzed and produce ROS, especially highly toxic free hydroxyl radicals, via Fenton reactions that may finally result in chronic hepatorenal diseases 56
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