We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Reactive oxygen metabolites in endotoxin-induced acute renal failure in rats.
- Authors
Walker, Patrick D.; Shah, Sudhir V.
- Abstract
Based on recent reports that reactive oxygen metabolites may play a role in endotoxin-induced injury in other tissues, we postulated that reactive oxygen metabolites may be important mediators of endotoxin-induced acute renal failure. Superoxide dismutase, a scavenger of superoxide, or catalase, which destroys hydrogen peroxide, did not protect against endotoxin-induced renal failure. Similarly, neither the hydroxyl radical scavenger dimethylthiourea nor the iron chelator deferoxamine (which presumably would act by preventing the generation of hydroxyl radical via the iron-catalyzed Haber-Weiss reaction) prevented the endotoxin-induced fall in renal function. In separate experiments, we found no increase in renal cortical lipid peroxidation (a marker of reactive oxygen metabolite-mediated tissue injury) in endotoxin-treated rats, providing further evidence against a role for reactive oxygen metabolites in endotoxin-induced renal injury. Finally, using the aminotriazole-induced inhibition of catalase (a measure of in vivo changes in the hydrogen peroxide generation) we found no evidence of enhanced hydrogen peroxide generation in the renal cortex in endotoxin- treated rats. Taken together, the data from these three separate experimental approaches suggest that reactive oxygen metabolites are not important mediators of endotoxin-induced acute renal failure.
- Subjects
REACTIVE oxygen species; ENDOTOXINS; ACUTE kidney failure; METABOLITES; KIDNEY diseases; DEFEROXAMINE
- Publication
Kidney International, 1990, Vol 38, Issue 6, p1125
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/ki.1990.322