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Am J Physiol Renal Physiol (July 12, 2001). doi:10.1152/ajprenal.0071.2001
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Articles in PresS, published online ahead of print July 12, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0071.2001
Submitted on March 1, 2001
Accepted on June 25, 2001

Scavenging of peroxynitrite ameliorates lipid peroxidation and DNA damage in experimental ischemic acute renal failure

Eisei Noiri1*, Akihide Nakao2, Koji Uchida3, Hirokazu Tsukahara4, Minoru Ohno5, Toshiro Fujita2, Sergey Brodsky6, and Michael Goligorsky6

1 Nephrology & Endocrinology, The Univ. of Tokyo, Tokyo, Tokyo, Japan; Medicine and Physiology, SUNY at Stony Brook, Stony Brook, NY, USA
2 Nephrology & Endocrinology, The Univ. of Tokyo, Tokyo, Tokyo, Japan
3 Lab. of Food and Biodynamics, Nagoya Univ., Nagoya, Aichi, Japan
4 Pediatrics, Fukui Medical Univ., Fukui, Fukui, Japan; Medicine and Physiology, SUNY at Stony Brook, Stony Brook, NY, USA
5 Cardiovascular Disease, The Univ. of Tokyo, Tokyo, Tokyo, Japan
6 Medicine and Physiology, SUNY at Stony Brook, Stony Brook, NY, USA

* To whom correspondence should be addressed. E-mail: noiri-tky{at}umin.ac.jp.

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 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 prior to 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.




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