title: (-)-Epicatechin prevents alterations in the metabolism of superoxide anion and nitric oxide in the hearts of L-NAME-treated rats.
abstract: The aim of this work was to evaluate the effects of (-)-epicatechin administration in the heart of a rat model with reduced NO production that follows a short-term treatment with L-NAME. Sprague-Dawley rats were treated for 4 d with L-NAME in the absence or presence of (-)-epicatechin in the diet. The redox status in cardiac tissue was improved by (-)-epicatechin administration. L-NAME treatment induced a decrease in NO synthase activity (-62%, p<0.05) and an increase in NADPH-dependent superoxide anion production (+300%, p<0.05) that were totally prevented by (-)-epicatechin administration. These effects of (-)-epicatechin were associated with a higher endothelial NO synthase phosphorylation at an activation site and a reduced expression of the regulatory subunit, p47(phox), suggesting the involvement of posttranslational mechanisms in (-)-epicatechin action. Thus, the (-)-epicatechin treatment would restore NO steady state levels in vivo through effects on both, its synthesis and degradation via the reaction with superoxide anion. The fact that (-)-epicatechin is commonly present in human diet makes this compound a reasonable explanation for the positive cardiovascular effects of a high consumption of fruits and vegetables.
authors.affiliation: Physical Chemistry and Institute of Molecular Biochemistry and Medicine, University of Buenos Aires (IBIMOL) - CONICET, School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina. barbara@ffyb.uba.ar.
authors.forename: Barbara
authors.initials: B
authors.lastname: Piotrkowski
authors.forename: Valeria
authors.initials: V
authors.lastname: Calabró
authors.forename: Mónica
authors.initials: M
authors.lastname: Galleano
authors.forename: César G
authors.initials: CG
authors.lastname: Fraga
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D002392:Catechin / Q000627:therapeutic use*; D003331:Coronary Vessels / Q000201:enzymology / Q000378:metabolism; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004789:Enzyme Activation; D005638:Fruit / Q000737:chemistry; D006352:Heart Ventricles / Q000201:enzymology* / Q000378:metabolism; D006973:Hypertension / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000819:agonists / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000737:chemistry / Q000378:metabolism*; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D013237:Stereoisomerism; D013481:Superoxides / Q000037:antagonists & inhibitors / Q000378:metabolism; D014675:Vegetables / Q000737:chemistry
chemical_list: D000959:Antihypertensive Agents; D013481:Superoxides; D009569:Nitric Oxide; D002392:Catechin; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1; D019331:NG-Nitroarginine Methyl Ester