'Til cell death do us part: Nitric oxide and mechanisms of hepatotoxicity

Peter K.M. Kim*, Brian S. Zuckerbraun, Leo E. Otterbein, Yoram Vodovotz, Timothy R. Billiar

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

19 Scopus citations


Like many juggernauts in biology, the elusive nature of nitric oxide (NO) sprints through the fields, sometimes the savior, at other times the scimitar. In the liver, which is the metabolic center of the organism, hepatocytes and immune cells trade blows using the reactive diatomic molecule NO to induce cellular damage under toxic conditions. In response, hepatocytes can utilize several mechanisms of NO to their protective advantage by prohibiting the activation of programmed cell death, a.k.a. apoptosis. The balance of these effects in this reactive milieu set the stage for the homeostatic response to cellular injury that determines whether hepatocytes will live, die, or regenerate. Insights that we and others have gained from the liver under pathologic conditions of stress can be applied to the understanding of cellular death mechanisms in other organs and tissues.

Original languageEnglish
Pages (from-to)11-15
Number of pages5
JournalBiological Chemistry
Issue number1
StatePublished - Jan 2004
Externally publishedYes


  • Apoptosis
  • Carbon monoxide
  • Caspase
  • FADD
  • Heme oxygenase
  • Hepatocyte
  • Liver
  • Necrosis
  • Nitric oxide
  • Nitric oxide synthase
  • cGMP


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