Role of NADPH oxidase-derived superoxide in reduced size liver ischemia and reperfusion injury
Section snippets
Animals
Wild type (wt) male C57Bl/6 mice (18–24 g) were purchased from Harlan while mice genetically deficient in the gp91phox sub-unit of NADPH oxidase (gp91−/−) on a C57B/6 background were obtained from Jackson Laboratories (Bar Harbor, ME) and generated as described previously [24]. All animals were maintained on a standard laboratory diet with free access to food and water until the time of the experiment.
Animal model of reduced size liver ischemia–reperfusion
Fasted (16–18 h) mice were anesthetized with intramuscular ketamine (150 mg/kg) and xylazine (7.5
Animal survival, tissue injury, and TNF-α expression following RSL + I/R
In a first series of studies, we wished to define what role superoxide (O2−) and TNF-α play in a model of RSL + I/R. Fig. 1 presents the 7 day mortality percentages of wt mice subjected to RLS + I/R or sham surgery. We found that all (100%) mice died within 3–5 days following the surgery as we have previously described [25], [26]. This increased mortality was preceded by substantial and significant increases in liver injury as measured by increased serum ALT levels at 3 h post surgery (Fig. 1).
Acknowledgements
Some of this work was supported by a grant from the NIH (DK43875).
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