Jun 1, 2002

Postischemic renal oxidative stress induces inflammatory response through PAF and oxidized phospholipids. Prevention by antioxidant treatment

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
Nuria LloberasJosep M Grinyó


Reperfusion injury is considered primarily an inflammatory response to oxidative stress. In vitro, oxygen free radicals induce the formation of oxidized phospholipids with platelet-activating factor (PAF) activity (PAF-like lipids). We examined the following: 1) whether PAF and PAF-like lipids are released during reperfusion; 2) the relationship between these phospholipids and oxidative damage on the one hand, and leukocyte recruitment in renal tissue on the other; and 3) whether antioxidant treatment influences the behavior of these phospholipids, the renal inflammatory response, and the outcome of postischemic acute renal failure. After 60 min of warm renal ischemia in rabbits, a release of PAF and, particularly, PAF-like lipids was seen in the first 15 min of reperfusion. In addition, the release of those phospholipids was associated with intense tissue DNA oxidation and with an increase in myeloperoxidase activity. Vitamin C was able to attenuate these postischemic oxidative changes, decrease PAF and PAF-like lipid levels, and, consequently, reduce myeloperoxidase activity. After 40 min of warm renal ischemia in rats, vitamin C treatment ameliorated renal function and structure. This is the first in vivo demonstration of th...Continue Reading

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Mentioned in this Paper

Kidney Function Tests
Systemic Inflammatory Response Syndrome
Renal Tissue
Kidney Failure, Acute
Antioxidant Effect
Peroxidase Activity
Oxidative Stress

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