Ethanol-induced apoptosis and oxidative stress in hepatocytes

Hajime Higuchi, Iwao Kurose, Shinzo Kato, Soichiro Miura, Hiromasa Ishii

Research output: Contribution to journalArticlepeer-review

74 Citations (Scopus)


This short review focuses on ethanol-induced oxidative stress and hepatocyte apoptosis. Apoptosis is increasingly recognized as a fundamental biological process that impacts on an early development, maturation, and acquisition of disease states of multicellular organisms. Although the occurrence of apoptosis has been identified for many decades, relatively recent acceptance of this principle is evidenced by remarkable increases in special conferences and presentations on this topic as well as its rapidly expanding volume of scientific literature. Oxidative stress is well recognized to be a key step in the pathogenesis of ethanol-associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Studies in our laboratory using a confocal laser scanning microscopic system strongly suggest that agents which inhibit ethanol-induced oxidative stress effectively attenuate hepatocyte death, i.e., apoptosis and necrosis. In addition, our investigations demonstrated that inhibitors of intracellular antioxidants exaggerate ethanol-associated hepatocyte apoptosis. Although the detailed mechanism still remains unknown, it is conceivable that an oxidant-dependent mechanism is largely involved in the process for ethanol-induced hepatocyte apoptosis.

Original languageEnglish
Pages (from-to)340A-346A
JournalAlcoholism: Clinical and Experimental Research
Issue number9 SUPPL.
Publication statusPublished - 1996 Dec 1


  • Dichlorofluorescein- Diacetate
  • Hoechst 33342
  • Laser Scanning Confocal Microscope
  • Monochlorobimane
  • Nick End Labeling

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health


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