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Inhibiting the elevated expression of GJ components in hepsin / mice reduces APAP toxicity by limiting oxidative stress in the liver To investigate GJ expression variations after APAP administration in wild-type and hepsin / mice, immunofluorescence staining for Cx32 was assessed at different time points

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Mitochondria generate the majority of cellular ROS as a byproduct of oxidative phosphorylation, and mitochondrial GSH is the primary defense against this constant oxidative burden

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