Acute oxidative stress is associated with cell proliferation in the mouse liver

FEBS Lett. 2006 Jul 10;580(16):3845-52. doi: 10.1016/j.febslet.2006.06.006. Epub 2006 Jun 15.


Oxidative stress is known to produce tissue injury and to activate various signaling pathways. To investigate the molecular events linked to acute oxidative stress in mouse liver, we injected a toxic dose of paraquat. Liver necrosis was first observed, followed by histological marks of cell proliferation. Concomitantly, activation of the MAP kinase pathway and increased levels of the anti-apoptotic protein Bcl-XL were observed. Gene expression profiles revealed that the differentially expressed genes were potentially involved in cell proliferation. These data suggest that paraquat-induced acute oxidative stress triggers the activation of regeneration-related events in the liver.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Bromodeoxyuridine
  • Cell Proliferation
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • DNA / biosynthesis
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Genes / genetics
  • Liver / cytology*
  • Liver / drug effects
  • Liver / metabolism*
  • Liver Regeneration / drug effects
  • Mice
  • Mice, Inbred C57BL
  • Necrosis
  • Oligonucleotide Array Sequence Analysis
  • Oxidative Stress*
  • Paraquat / pharmacology
  • Phosphorylation
  • Time Factors
  • Up-Regulation / genetics
  • bcl-X Protein / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Cyclic AMP Response Element-Binding Protein
  • bcl-X Protein
  • DNA
  • Alanine Transaminase
  • Extracellular Signal-Regulated MAP Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Bromodeoxyuridine
  • Paraquat