Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 232-237 |
| Number of pages | 6 |
| Journal | Archives of Biochemistry and Biophysics |
| Volume | 484 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2009 Apr 15 |
| Externally published | Yes |
Keywords
- Cytokines
- Free radicals
- Hemoglobin
- Liver ischemia
- NF-κB
- Peroxynitrite
- Superoxide
- TNF
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology