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Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential.

Abstract：

:Acetaminophen (APAP) hepatotoxicity is characterized by an extensive oxidative stress. However, its source, pathophysiological role and possible therapeutic potential if targeted, have been controversially described. Earlier studies argued for cytochrome P450-generated reactive oxygen species (ROS) during APAP metabolism, which resulted in massive lipid peroxidation and subsequent liver injury. However, subsequent studies convincingly challenged this assumption and the current paradigm suggests that mitochondria are the main source of ROS, which impair mitochondrial function and are responsible for cell signaling resulting in cell death. Although immune cells can be a source of ROS in other models, no reliable evidence exists to support a role for immune cell-derived ROS in APAP hepatotoxicity. Recent studies suggest that mitochondrial targeted antioxidants can be viable therapeutic agents against hepatotoxicity induced by APAP overdose, and re-purposing existing drugs to target oxidative stress and other concurrent signaling events can be a promising strategy to increase its potential application in patients with APAP overdose.

journal_name

Redox Biol

journal_title

Redox biology

authors

Du K,Ramachandran A,Jaeschke H

doi

10.1016/j.redox.2016.10.001

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

148-156

issn

2213-2317

pii

S2213-2317(16)30173-2

journal_volume

10

pub_type

杂志文章,评审

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