X-Message-Number: 11903
Date: Sun, 6 Jun 1999 03:38:34 -0700 (PDT)
From: Doug Skrecky <>
Subject: pyruvate protects glycerol induced injury

  Salahudeen AK.  Clark EC.  Nath KA.
  Department of Medicine, University of Minnesota, Minneapolis 55455.
  Hydrogen peroxide-induced
  renal injury. A protective role for pyruvate in vitro and in
  Journal of Clinical Investigation.  88(6):1886-93, 1991 Dec.
  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.

Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=11903