Hepatocellular protection by nitric oxide or nitrite in ischemia and reperfusion injury

Yuta Abe, Ian Hines, Gazi Zibari, Matthew B. Grisham

研究成果: Review article査読

33 被引用数 (Scopus)

抄録

Ischemia and reperfusion (I/R)-induced liver injury occurs in several pathophysiological disorders including hemorrhagic shock and burn as well as resectional and transplantation surgery. One of the earliest events associated with reperfusion of ischemic liver is endothelial dysfunction characterized by the decreased production of endothelial cell-derived nitric oxide (NO). This rapid post-ischemic decrease in NO bioavailability appears to be due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide or both. This review presents the most current evidence supporting the concept that decreased bioavailability of NO concomitant with enhanced production of reactive oxygen species initiates hepatocellular injury and that endogenous NO or exogenous NO produced from nitrite play important roles in limiting post-ischemic tissue injury.

本文言語English
ページ(範囲)232-237
ページ数6
ジャーナルArchives of Biochemistry and Biophysics
484
2
DOI
出版ステータスPublished - 2009 4月 15
外部発表はい

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学

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