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Indeed, a burst in H 2 O 2 production in mitochondria may be required to feedback and deactivate Odh and possibly Pdh to curtail further H 2 O 2 production by either Odh and Pdh or the respiratory complexes (Figure 2) (Young et al., 2000

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However, chronic deletion of Parkin renders animals resistant to APAP [82], possibly due to development of compensatory and adaptive mechanisms for the chronic loss of Parkin, which may contribute to the resistance to APAP-induced liver injury [82]

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