Cardiac oxidative modifications in fructose overload rats and prevention by (-)-epicatechin.

PIOTRKOWSKI B; CALABRÓ V; ASCHETTINO G; FISCHERMAN L; VAZQUEZ PRIETO MA; GALLEANO M; FRAGA CG

Alba

Congreso; A Joint Meeting for the Oxygen Club of California and the University of Turin; 2012

The Oxygen Club of California and the University of Turin

The purpose of this study was to evaluate the effects of (-)-epicatechin (EC) supplementation on oxidative modifications in the heart of rats subjected to a model of metabolic syndrome. Male Sprague-Dawley rats were divided into three groups and received for 8 w: i) control diet and tap water (C); ii) control diet and 10% (w/v) fructose in the drinking water (F), and iii) 10% (w/v) fructose in the drinking water, and the diet supplemented with EC (20 mg/kg BW/d) (FEC).  Systolic blood pressure in rats with fructose overload was significantly higher than in control rats and EC prevented that increase (C=130±4; F=142±3*; FEC=133±3 mmHg; *p<0.05 with respect to C and FEC). All the following parameters were assessed in heart homogenates. Superoxide production, evaluated as SOD-inhibited NADH-induced lucigenin chemiluminescence, was increased in F with respect to C group. Rats receiving EC in the diet did not showed that increase (C= 8.1±0.1; F=10.2±0.2*; FEC= 5.8±0.2; *p<0.05 with respect to C and FEC). In accordance, NOX4 expression was significantly higher in F group with respect to C and FEC (20% and 15%, respectively; p<0.05). Both, superoxide dismutase and glutathione peroxidase activities were significantly decreased in F group compared to control (41% and 48%, respectively), and EC treatment prevented the decrease in both enzymes activities. In summary, these results show that EC supplementation prevented the effects associated with fructose-overload treatment in the heart, and this prevention could be interpreted as a protection from increased oxidant production related to metabolic syndrome