Abstract
Background: Mitochondria go through frequent cycles of fusion and fission, a process required for mitochondrial quality control by eliminating ROS damaged mitochondria through mitophagy. Acetaminophen (APAP) overdose causes liver injury in animals and humans usually by mitochondria damage, which needed further study. Toxicity is mediated by the metabolism of APAP to the reactive metabolite N acetyl-p-benzoquinone imine, which forms adducts on cellular proteins in mitochondria. The aim of the current study is to assess the changes between oxidative stress and companied mitophagy in a rodent model which mimics APAP-induced liver injury (AILI) in humans.
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