498-504 Molina LAJP 1427

Free radicals produce detrimental effects on target molecules, like increased lipid, protein and DNA peroxidation, which can be inhibited or delayed by antioxidant substances. D-003 is a mixture of high molecular weight sugarcane wax acids that has shown to inhibit lipid peroxidation (LP) in animal models and healthy volunteers. Grape seed extracts (GSE), rich in flavonoids, have demonstrated potent and effective antioxidant effects in experimental and clinical studies. No previous study, however, has compared the in vivo antioxidant effects of D-003 and GSE. This study was undertaken in order to compare the effects of oral treatment with D-003 and GSE on plasma and liver LP in the rat. Male Wistar rats were distributed into 5 groups: a control treated with acacia gum/water vehicle, two treated with D-003 and two with GSE, both at 25 and 250 mg/kg. After 4 weeks on treatment, effects on plasma LP were assessed by measuring the concentrations of malondyaldehide (MDA) and total peroxides, and effects on liver LP by determining the MDA concentrations generated with the enzymatic (NADPH/ADP/ClFe3) and non-enzymatic (FeSO4/ ascorbate/KH2PO4) oxidant systems. Compared with the controls, D-003 (25 and 250 mg/kg) significantly (p < 0.001), but modestly, reduced plasma MDA (25.4% and 35.6%, respectively), whereas GSE at 250 mg/kg, not at 25 mg/kg, lowered MDA significantly (p < 0.001) and modestly (22.4%). At 25 mg/kg the effects of D-003 were greater than (p < 0.001) those of GSE, but at 250 mg/kg were similar. D-003 and GSE at 25 and 250 mg/kg decreased significantly (p < 0.001) plasma peroxides. With the highest dose, the reductions with GSE (62.1%) were greater (p < 0.001) than with D-003 (49.1%). In the liver, D-003 (25 mg/kg) reduced significantly (p < 0.0001), but modestly, the MDA concentrations generated with the enzymatic (28.4%) and the non-enzymatic system (55.8 %), effects that increased noticeably at 250 mg/kg, lowering significantly (p < 0.0001) and markedly MDA levels by 77.4% (enzymatic system) and 79.1% (non-enzymatic system). At 25 mg/kg, GSE reduced (p < 0.0001) modestly (15.0%) MDA generated with the non-enzymatic system only, while at 250 mg/kg, it decreased significantly (p < 0.0001) and markedly MDA concentrations generated with the enzymatic (89.4%) and the non-enzymatic system (91.2%), more (p < 0.01) than with D-003. D-003 and GSE did not change significantly the activity of GPX, CAT and GSHR compared with the controls. In conclusion, D-003 and GSE orally administered to rats for 4 weeks inhibited LP in plasma and liver. At the highest dose, the effects of both treatments on plasma MDA were modest and similar, while the effects on total peroxides were moderate, and greater with GSE. The effects of both treatments on liver LP induced with both systems were significant and marked, D-003 was more effective at 25 mg/kg, and GSE at the highest dose, although the differences between both treatments were modest. No effects on antioxidant enzymes were observed.