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Research Article Free access | 10.1172/JCI115511

Hydrogen peroxide-induced renal injury. A protective role for pyruvate in vitro and in vivo.

A K Salahudeen, E C Clark, and K A Nath

Department of Medicine, University of Minnesota, Minneapolis 55455.

Find articles by Salahudeen, A. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Minnesota, Minneapolis 55455.

Find articles by Clark, E. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Minnesota, Minneapolis 55455.

Find articles by Nath, K. in: JCI | PubMed | Google Scholar

Published December 1, 1991 - More info

Published in Volume 88, Issue 6 on December 1, 1991
J Clin Invest. 1991;88(6):1886–1893. https://doi.org/10.1172/JCI115511.
© 1991 The American Society for Clinical Investigation
Published December 1, 1991 - Version history
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Abstract

Hydrogen peroxide (H2O2) contributes to renal cellular injury. alpha-Keto acids nonenzymatically reduce H2O2 to water while undergoing decarboxylation at the 1-carbon (1-C) position. We examined, in vitro and in vivo, the protective role of sodium pyruvate in H2O2-induced renal injury. Pyruvate effectively scavenged H2O2 in vitro, and suppressed H2O2-induced renal lipid peroxidation. Injury to LLC-PK1 cells induced by hydrogen peroxide was attenuated by pyruvate to an extent comparable to that seen with catalase. Studies utilizing [1-14C]pyruvate further demonstrated 1-C decarboxylation concurrent with cytoprotection by pyruvate from H2O2-induced injury. Pyruvate was also protective in vivo. Infusion of pyruvate before and during the intrarenal infusion of H2O2 attenuated H2O2-induced proteinuria. Systemic administration of pyruvate was also protective in the glycerol model of acute renal failure, a model also characterized by increased generation of H2O2. These findings indicate that pyruvate, a ubiquitous alpha-keto acid, scavenges H2O2 and protects renal tissue in vitro and in vivo from H2O2-mediated injury. These data suggest a potential therapeutic role for pyruvate in diseases in which increased generation of H2O2 is incriminated in renal damage.

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