X-Message-Number: 15777
Date: Thu, 1 Mar 2001 09:15:21 -0800 (PST)
From: Doug Skrecky <>
Subject: grape bioflavanoids reduce glycerol toxicity

  Reversal of experimental
  myoglobinuric acute renal failure with
  bioflavonoids from seeds of grape.
  Renal Failure.  22(3):255-66, 2000 May.
  Rhabdomyolysis may account for about 10% of all cases of
  acute renal failure (ARF). This study was performed to
  explore the protective influence of proanthocyanidins from seeds of grape in
  an experimental model of myoglobinuric ARF.
  Rats were injected with 50% glycerol (8 mL/kg, im) followed immediately and
 daily in the next three days by ip proanthocyanidins (20 mg/kg) or saline.
  After 96 h rats were sacrificed and kidney morphology, kidney cortex
  peptidase activities, and malondialdehyde (MDA) content were determined. A
  moderate renal failure was produced by glycerol injection with blood urea of
  31.8+/-11.0 vs. 7.68+/-0.24 m mol/L, and serum creatinine of 153. +/-38.2 vs.
  39.6+/-9.0 micromol/L, in glycerol-induced ARF vs. control rats,
  respectively. Rats that received proanthocyanidins in addition to glycerol
  had significantly lower (p < 0.01) blood urea and serum creatinine levels
  compared to those receiving glycerol alone. These functional differences
  between the glycerol and glycerol plus proanthocianidins groups were also
  confirmed histologically. Kidney cortex dipeptidylpeptidase IV (DPP IV)
  activity was not significantly changed in glycerol-induced ARF, however,
  markedly increased after proanthocyanidins treatment. Kidney cortex
  malondialdehyde content was found significantly increased in glycerol-induced
  ARF over control level, and was markedly reduced by proanthocyanidin
  treatment. Taken together, these results provide strong evidence for the
  protective role of proanthocyanidins from seeds of grape in glycerol-induced
  ARF. The effect is probably due to the antioxidant activity of
  proanthocyanidins and to increased expression of kidney cortex DPP IV with
  effective degradation of TNF-alpha. This may provide therapeutic
  opportunities of preventing and/or treating myoglobinuric
  ARF in humans.

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