Acrolein, a highly toxic aldehyde generated under oxidative stress in vivo, aggravates the mouse liver damage after acetaminophen overdose

Biomedical Research
Tomoya AraiRyushin Mizuta

Abstract

Although acetaminophen-induced liver injury in mice has been extensively studied as a model of human acute drug-induced hepatitis, the mechanism of liver injury remains unclear. Liver injury is believed to be initiated by metabolic conversion of acetaminophen to the highly reactive intermediate N-acetyl p-benzoquinoneimine, and is aggravated by subsequent oxidative stress via reactive oxygen species (ROS), including hydrogen peroxide (H2O2) and the hydroxyl radical (•OH). In this study, we found that a highly toxic unsaturated aldehyde acrolein, a byproduct of oxidative stress, has a major role in acetaminophen-induced liver injury. Acetaminophen administration in mice resulted in liver damage and increased acrolein-protein adduct formation. However, both of them were decreased by treatment with N-acetyl-L-cysteine (NAC) or sodium 2-mercaptoethanesulfonate (MESNA), two known acrolein scavengers. The specificity of NAC and MESNA was confirmed in cell culture, because acrolein toxicity, but not H2O2 or •OH toxicity, was inhibited by NAC and MESNA. These results suggest that acrolein may be more strongly correlated with acetaminophen-induced liver injury than ROS, and that acrolein produced by acetaminophen-induced oxidative stres...Continue Reading

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Citations

Sep 7, 2016·The Journal of Veterinary Medical Science·Ryo Koyama, Ryushin Mizuta
Sep 23, 2016·Genes to Cells : Devoted to Molecular & Cellular Mechanisms·Ryo KoyamaRyushin Mizuta
Oct 11, 2017·Current Pharmacology Reports·Sean S Davies, Linda S Zhang
Jul 2, 2017·Toxicological Sciences : an Official Journal of the Society of Toxicology·Jianbo ZhangShana J Sturla
Mar 25, 2021·The Science of the Total Environment·Sebastian HegerMiaomiao Du
Dec 19, 2016·Chemical Research in Toxicology·Richard M LoPachinTerrence Gavin

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