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A secondary effect of this stress is activation of Nrf2 and its target genes resulting in compensatory higher GSH levels and induction of antioxidant genes in the livers of these mice, which makes these livers more resistant to additional acute stress such as APAP toxicity [151]

It catalyzes the reduction of hydrogen peroxide (H2O2), hydroperoxides and lipid hydroperoxides via reduced GSH (12)

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