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Departments of 1 Nephrology and Endocrinology and 5 Cardiovascular Disease, The University of Tokyo, Tokyo 113 - 8655; 3 Laboratory of Food and Biodynamics, Nagoya University, Nagoya 464-8601; 4 Department of Pediatrics, Fukui Medical University, Fukui, Japan 910-1193; and 2 Departments of Medicine and Physiology, State University of New York at Stony Brook, Stony Brook, New York 11794-8152
First Published July 12, 2001;
10.1152/ajprenal.0071.2001.
Generation of reactive oxygen species and
nitric oxide in hypoxia-reperfusion injury may form a cytotoxic
metabolite, peroxynitrite, which is capable of causing lipid
peroxidation and DNA damage. This study was designed to examine the
contribution of oxidative and nitrosative stress to the renal damage in
ischemic acute renal failure (iARF). iARF was initiated in rats
by 45-min renal artery clamping. This resulted in lipid peroxidation,
DNA damage, and nitrotyrosine modification confirmed both by Western
and immunohistochemical analyses. Three groups of animals were randomly
treated with an inhibitor of inducible nitric oxide synthase (NOS),
L-N6-(1-iminoethyl)lysine
(L-Nil), cell-permeable lecithinized superoxide dismutase
(SOD), or both. Each treatment resulted in amelioration of renal
dysfunction, as well as reduced nitrotyrosine formation, lipid
peroxidation, and DNA damage, thus suggesting that peroxynitrite rather
than superoxide anion is responsible for lipid peroxidation and DNA
damage. Therefore, in a separate series of experiments, a scavenger of
peroxynitrite, ebselen, was administered before the reperfusion period.
This treatment resulted in a comparable degree of amelioration of iARF.
In conclusion, the present study provides the first attempt to
elucidate the role of peroxynitrite in initiation of the cascade of
lipid peroxidation and DNA damage to ischemic kidneys. The
results demonstrate that L-Nil , lecithinized SOD, and
ebselen treatments improve renal function due to their suppression of
peroxynitrite production or its scavenging, consequently preventing
lipid peroxidation and oxidative DNA damage.
4-hydroxy-2-nonenal; 8-hydroxy-2'-deoxyguanosine; L-N6-(1-iminoethyl)lysine; lecithinized superoxide dismutase; ebselen
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