Protective Effects of Grape Juice on Vascular Damage Induced by Chlorine Free Radical in Rats.

Grapes and their derivatives have antioxidant and cardioprotective properties. Therefore, we hypothesized that grape juice (GJ) could improve vascular oxidative damage caused by chlorine radicals (OCl-), which are excessively produced in vascular tissue during cardiovascular diseases (mainly diabetes and hypertension). The antioxidant capacity of GJ was analyzed by an electrochemical method, followed by administration in rats (100 or 300 mg/kg/d, via the oral) for seven days. Then, rats were sacrificed, and their aortas were isolated and subjected to isometric recordings or immuno-histochemical analyses with or without exposure to OCl- (5, 20, or 100 µM, 60 min). Concentration-effect curves for acetylcholine (ACh) and sodium nitroprusside (SNP) were derived to analyze endothelium-dependent or independent vasore-laxation. The GJ presented with high antioxidant capacity, and treatment with GJ did not alter vascular relaxation induced by ACh or SNP. After exposure to OCl-, endothelium-denuded arteries showed preserved relaxation with SNP, whereas endothelium-intact arteries showed reduced relaxation with ACh. OCl- at various concentrations induced significantly decreased relaxation of arteries (80.6±4.2%, 55.4±4.7%, and 28.1±5.9%, respectively) vs. control arteries (96.8±2.4%). However, treatment with GJ prevented loss in relaxation caused by 5 and 20 µM OCl- and improved relaxation after exposure to 100 µM OCl-. Exposure to OCl- induced increased nitrotyrosine immunostaining of endothelial cell layers, which was improved by GJ treatment. Altogether, vascular damage caused by OCl- was prevented by treatment with GJ, and GJ prevented nitrosative stress in these vessels.

Paracetamol-induced metabolic and cardiovascular changes are prevented by exercise training.

Paracetamol (PAR) is the most frequently consumed non-prescription drug, yet it is well known to induce toxicity. Here, we have evaluated the effects of exercise training on vascular dysfunction induced by PAR. Rats were distributed among four groups: (a) Sedentary; (b) Exercise; (c) Sedentary+PAR; and (d) Exercise+PAR. The exercise comprised swimming 50 min/d, 5 d/wk for 6 weeks (+PAR in the last 2 weeks, at 400 mg/kg/d/p.o.). After killing, the rats' blood and aortas were collected for biochemical analysis of hepatic transaminases, TBARs reaction, glutathione, glutathione reductase, SOD, and catalase. In vitro vascular relaxation was measured using acetylcholine and sodium nitroprusside in the presence or absence of tiron (an antioxidant). Vascular protein expression (eNOS and sGC) also were analysed. Increased transaminases after PAR treatment were found to be reduced by exercise. Vasodilation was impaired by PAR only in the sedentary group. Exercise prevented alterations in lipoperoxidation and glutathione levels after PAR exposure. Glutaathione reductase and SOD also were increased by PAR but were normalized in the exercised group. Catalase activity and protein expressions did not change in any group. PAR treatment caused impairment in both vasodilation and redox balance; however, exercise training prevented the vascular and redox system dysfunction induced by PAR treatment.