Changes in Hepatic TNF-α Levels, Antioxidant Status, and Oxidation Products after Renal Ischemia/Reperfusion Injury in Mice

Background. Ischemia/reperfusion (I/R) injury induces an inflammatory response and production of reactive oxygen species (ROS), which affects the organs remote to the sites of I/R. The aim was to assess the hepatic changes after renal I/R injury. Materials and methods. Twenty mice were subjected to...

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Published in:The Journal of surgical research 2002-10, Vol.107 (2), p.234-240
Main Authors: Serteser, Mustafa, Koken, Tulay, Kahraman, Ahmet, Yilmaz, Keriman, Akbulut, Gokhan, Dilek, Osman Nuri
Format: Article
Language:English
Subjects:
Animals
antioxidant enzymes
Biological and medical sciences
Catalase - metabolism
Investigative techniques, diagnostic techniques (general aspects)
Ischemia - metabolism
Kidney - blood supply
Lipid Peroxidation
liver
Liver - metabolism
Male
Medical sciences
Mice
myeloperoxidase
oxidation
Oxidation-Reduction
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Peroxidase - metabolism
Reactive Oxygen Species
renal ischemia
reperfusion
Reperfusion Injury - metabolism
Superoxide Dismutase - metabolism
TNF-α
Tumor Necrosis Factor-alpha - analysis
Tumor Necrosis Factor-alpha - biosynthesis
Urinary system
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Summary:Background. Ischemia/reperfusion (I/R) injury induces an inflammatory response and production of reactive oxygen species (ROS), which affects the organs remote to the sites of I/R. The aim was to assess the hepatic changes after renal I/R injury. Materials and methods. Twenty mice were subjected to either sham operation or varying degrees of renal I/R injury. Hepatic TNF-α levels, myeloperoxidase (MPO), superoxide dismutase (SOD), and catalase (CAT) activities and reduced glutathione (GSH) levels, thiobarbituric acid-reactive substances (TBARS), and protein carbonyl levels were evaluated to show hepatic response to renal I/R injury. Results. Hepatic tumor necrosis factor-alpha levels were found to be increased significantly after 30 min ischemia–1 h reperfusion and remained elevated through 60 min ischemia–1 h reperfusion. Supporting the neutrophil recruitment, about 10-fold increase in MPO activity was detected after 30 min ischemia–1 h reperfusion. Antioxidant enzymes were detected to be decreased after 30 min ischemia–1 h reperfusion and reached to the minimum levels after 60 min ischemia–1 h reperfusion. Decreased levels of GSH and increased levels of TBARS and protein carbonyls after 60 min ischemia–1 h reperfusion supported the ROS-mediated biomolecular alterations. Conclusions. A minumum of 30 min ischemia–1 h reperfusion is enough to elicit remote effects of renal I/R injury. Care should be taken to protect other organs remote from I/R sites especially during renal surgery.
ISSN:0022-4804
1095-8673
DOI:10.1006/jsre.2002.6513