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Although not entirely known, the mechanism(s) of elevation of GGT activity in patients with chronic liver disease of various etiologies may involve not only a passive release of the enzyme from the injured cells but also an accelerated release kinetics due to either increased intracellular synthesis or enhanced release into the bloodstream of GGT molecules expressed on cell surface [19]

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Mitochondrial complex I ROS production and redox signaling in hypoxia

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