Catechin, a natural antioxidant protects against rhabdomyolysis-induced myoglobinuric acute renal failure

Pharmacol Res. 2003 Nov;48(5):503-9. doi: 10.1016/s1043-6618(03)00207-x.


Rhabdomyolysis-induced myoglobinuric acute renal failure accounts for about 10-40% of all cases of acute renal failure (ARF). Reactive oxygen intermediates have been demonstrated to play an etiological role in myoglobinuric renal failure. This study was performed to explore the protective effect of catechin-a natural antioxidant in an experimental model of myoglobinuric ARF in rats. Four groups of rats were employed in this study, group 1 served as control, group 2 was given 50% glycerol (8 ml kg(-1), i.m.), group 3, glycerol plus catechin (40 mg kg(-1), p.o. for 4 days, twice a day) and group 4 was given only catechin (40 mg kg(-1), p.o.), respectively. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen (BUN), creatinine, and urea clearance. The oxidative stress was measured by renal malondialdehyde (MDA) levels, reduced glutathione levels and by enzymatic activity of catalase, glutathione reductase (GR) and superoxide dismutase (SOD). Glycerol administration resulted in a marked renal oxidative stress, significantly deranged the renal functions as well as renal morphology. All these factors were significantly improved by catechin treatment. Catechin, due to its antioxidative activity, reduced the toxicity of myoglobin in the renal tissues, and thus exerted a renoprotective effect in this rhabdomyolysis mimicking model.

MeSH terms

  • Acute Kidney Injury / drug therapy*
  • Acute Kidney Injury / pathology
  • Animals
  • Antioxidants / pharmacology*
  • Catalase / metabolism
  • Catechin / pharmacology*
  • Glutathione / metabolism
  • Glutathione Reductase / metabolism
  • Kidney / pathology
  • Kidney Function Tests
  • Lipid Peroxidation / drug effects
  • Male
  • Myoglobinuria / drug therapy*
  • Oxidation-Reduction
  • Oxidative Stress / drug effects
  • Rats
  • Rats, Wistar
  • Rhabdomyolysis / drug therapy*
  • Superoxide Dismutase / metabolism
  • Thiobarbituric Acid Reactive Substances / metabolism


  • Antioxidants
  • Thiobarbituric Acid Reactive Substances
  • Catechin
  • Catalase
  • Superoxide Dismutase
  • Glutathione Reductase
  • Glutathione