Increased generation of reactive oxygen species in isolated rat fatty liver during postischemic reoxygenation

Citation
B. Nardo et al., Increased generation of reactive oxygen species in isolated rat fatty liver during postischemic reoxygenation, TRANSPLANT, 71(12), 2001, pp. 1816-1820
Citations number
31
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
TRANSPLANTATION
ISSN journal
00411337 → ACNP
Volume
71
Issue
12
Year of publication
2001
Pages
1816 - 1820
Database
ISI
SICI code
0041-1337(20010627)71:12<1816:IGOROS>2.0.ZU;2-U
Abstract
Background, Whether fatty infiltration of the liver influences the generati on of reactive oxygen species (ROS) during reperfusion is unclear. Thus, th is study aimed to compare the ROS formation that occurs during postanoxic r eoxygenation in isolated normal and fatty livers. Methods, Isolated livers from fed Sprague-Dawley rats with normal or fatty livers induced by a choline-deficient diet were reperfused at 37 degreesC f or 60 min with an oxygenated medium containing 10 muM of lucigenin after 1 hr of warm ischemia, Superoxide anion generation was assessed by the chemil uminescence (CLS) signal emitted from the organ surface. The hepatic conten t of malondialdehyde (MDA) and glutathione was determined at the end of rep erfusion. Tissue injury was evaluated by the liver histology and the alanin e aminotransferase (ALT) release in the perfusate, Results. CLS started rapidly with reoxygenation and it diffused to the whol e organ in both groups. However, CLS emission was significantly higher in f atty liver (after 10 min: 812.425+/-39.898 vs. 294.525+/-21.068 photons/ cm (2)/sec; P<0.01), A greater concentration of MDA was measured at the end of reoxygenation in fatty liver. Finally, the liver histology and the ALT rel ease indicated a greater injury in steatotic than normal liver. Conclusions. The CLS technique allows a direct visualization and comparison of ROS generation from the organ surface. Fatty infiltration increases ROS generation in the liver during postischemic reoxygenation, likely leading to the greater lipid peroxidation observed in these experiments. The increa sed oxidative stress may contribute to the reduced tolerance of steatotic l ivers to ischemia-reperfusion injury.