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The role of Kupffer cell oxidant production in early ethanol-induced liver disease.

Authors
  • Wheeler, M D
  • Kono, H
  • Yin, M
  • Nakagami, M
  • Uesugi, T
  • Arteel, G E
  • Gäbele, E
  • Rusyn, I
  • Yamashina, S
  • Froh, M
  • Adachi, Y
  • Iimuro, Y
  • Bradford, B U
  • Smutney, O M
  • Connor, H D
  • Mason, R P
  • Goyert, S M
  • Peters, J M
  • Gonzalez, F J
  • Samulski, R J
  • And 1 more
Type
Published Article
Journal
Free Radical Biology and Medicine
Publisher
Elsevier
Publication Date
Dec 15, 2001
Volume
31
Issue
12
Pages
1544–1549
Identifiers
PMID: 11744328
Source
Medline
License
Unknown

Abstract

Considerable evidence for a role of Kupffer cells in alcoholic liver disease has accumulated and they have recently been shown to be a predominant source of free radicals. Several approaches including pharmacological agents, knockout mice, and viral gene transfer have been used to fill critical gaps in understanding key mechanisms by which Kupffer cell activation, oxidant formation, and cytokine production lead to liver damage and subsequent pathogenesis. This review highlights new data in support of the hypothesis that Kupffer cells play a pivotal role in hepatotoxicity due to ethanol by producing oxidants via NADPH oxidase.

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