Nitric oxide and redox regulation in the liver: Part I. General considerations and redox biology in hepatitis.

Published

Journal Article (Review)

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiologic processes, including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In Part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In Part II of this review, we will review oxidative stress in common pathophysiologic conditions, including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis, and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.

Full Text

Duke Authors

Cited Authors

  • Diesen, DL; Kuo, PC

Published Date

  • July 2010

Published In

Volume / Issue

  • 162 / 1

Start / End Page

  • 95 - 109

PubMed ID

  • 20444470

Pubmed Central ID

  • 20444470

Electronic International Standard Serial Number (EISSN)

  • 1095-8673

Digital Object Identifier (DOI)

  • 10.1016/j.jss.2009.09.019

Language

  • eng

Conference Location

  • United States