Renal Modifications Induced by Fructose Overload in Rats: Prevention by Dietary (-)-Epicatechin Administration

PRINCE, PD; VÁZQUEZ PRIETO, MA; GEREZ, EM; FRAGA, CG; GALLEANO, M

London

Congreso; 16th Biennial Meeting of the Society for Free Radical Research International; 2012

Metabolic syndrome is a risk factor for kidney disease. This study evaluated the effects of (-)-epicatechin (EC) supplementation on oxidative alterations and inflammation in the kidney of rats subjected to a model of metabolic syndrome. Male Sprague-Dawley rats were divided into three groups: control group (C) receiving control diet and tap water; fructose group (F)  receiving control diet and 10% (w/v)  fructose in the drinking water and fructose + (-)-epicatechin group (F+EC) receiving fructose and the diet supplemented with EC (20 mg/kg BW/d). Fructose overload caused a significant increase in thiobarbituric acid reactive substances (TBARS) in renal cortex, which was prevented by EC (C=0.98±0.07; F=1.27±0.10* and F+EC=0.91±0.07 mmol MDA/mg protein; *p<0.05 respect to C and F+EC). SOD-inhibited NADPH-induced lucigenin chemiluminescence was assayed in renal cortex homogenates as an index of superoxide anion production. F group showed a significant increase in this parameter that was prevented by EC (C=3.3±0.7; F=6.9±1.1* and F+EC=2.1±0.9 AU/mg protein; *p<0.05 respect to C and F+EC). Among the enzymatic antioxidant defenses, glutathione peroxidase and Cu/Zn SOD activities were increased in F group (27% and 33%, respectively), EC had no effect on both activities. Catalase and Mn-SOD activities were not affected by the treatments. Expression of inducible nitric oxide synthase (iNOS) by western blotting was evaluated as an inflammatory marker and resulted significantly increased in the renal cortex of fructose overload animals. EC avoided that increase (C=10.1±7.0; F=100.0±24.6* and F+EC=36.5±17.7 AU; *p<0.05 respect to C and F+EC). These findings suggest that EC administration would have protective effects ameliorating oxidative alterations and inflammation that contribute to kidney disease in the metabolic syndrome.