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

Abdulla K. Salahudeen, Edward C. Clark, Karl A. Nath

Research output: Contribution to journalArticlepeer-review

214 Scopus citations


Hydrogen peroxide (H2O2) contributes to renal cellular injury. α-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 α-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.

Original languageEnglish (US)
Pages (from-to)1886-1893
Number of pages8
JournalJournal of Clinical Investigation
Issue number6
StatePublished - 1991


  • Kidney
  • Oxidant stress
  • Proteinuria
  • Scavenger
  • α-keto acids

ASJC Scopus subject areas

  • Medicine(all)


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