title: Enhanced myocardial vitamin C accumulation in left ventricular hypertrophy in rats is not attenuated with transition to heart failure.
abstract: Indirect observations are compatible with cardiac vitamin C deficiency as one contributory factor to oxidative stress in heart failure, but data on ventricular vitamin C content are lacking. Here, we used the well established model of aortic-banded rats at the stage of compensated hypertrophy (6 weeks after banding) and at the transition to cardiac failure (22 weeks after banding) to analyze vitamin C, vitamin E, protein carbonyls and malondialdehyde tissue content together with the respective plasma concentrations. Furthermore, we investigated the expression of the vitamin C transporters SVCT1 and SVCT2 in the left ventricle (LV). Aortic-banded rats, independently from their age, had higher malondialdehyde and protein carbonyl levels in plasma and LV tissue compared to sham-operated animals indicating increased oxidative stress. Plasma vitamin C remained unaffected from cardiac overload, while LV vitamin C was elevated in both stages of hypertrophy together with an increased expression of the vitamin C transporter SVCT2 suggesting increased vitamin C uptake. The levels of antioxidants and lipid peroxides were similar 6 and 22 weeks after aortic banding. Therefore, the accumulation of vitamin C in compensated hypertrophy and in decompensated failure excludes cardiac vitamin C deficiency as a primary factor to oxidative stress in this model.
authors.affiliation: Institute of Pathophysiology, Martin-Luther-University Halle-Wittenberg, Germany. susanne.rohrbach@medizin.uni-halle.de
authors.forename: Susanne
authors.initials: S
authors.lastname: Rohrbach
authors.forename: Antonio
authors.initials: A
authors.lastname: Martin
authors.forename: Bernd
authors.initials: B
authors.lastname: Niemann
authors.forename: Antonio
authors.initials: A
authors.lastname: Cherubini
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D015153:Blotting, Western; D004195:Disease Models, Animal; D006333:Heart Failure / Q000378:metabolism*; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000097:blood; D020778:Matrix Metalloproteinase 2 / Q000097:blood; D009206:Myocardium / Q000378:metabolism*; D029363:Organic Anion Transporters, Sodium-Dependent / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D050050:Protein Carbonylation / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D060347:Sodium-Coupled Vitamin C Transporters; D027981:Symporters / Q000378:metabolism; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood; D014810:Vitamin E / Q000097:blood
chemical_list: D029363:Organic Anion Transporters, Sodium-Dependent; D060347:Sodium-Coupled Vitamin C Transporters; D027981:Symporters; D019715:Tissue Inhibitor of Metalloproteinase-1; D014810:Vitamin E; D008315:Malondialdehyde; D020778:Matrix Metalloproteinase 2; D001205:Ascorbic Acid