title: Aortic-banding induces myocardial oxidative stress and changes in concentration and activity of antioxidants in male Wistar rats.
abstract: Myocardial activity and gene expression of antioxidant defenses and oxidative damage were examined in an experimental model of pressure overload hypertrophy. Male Wistar rats were divided into abdominal aortic-banded or sham-operated groups. After 30 days, arterial pressure and heart rate were measured. Heart, lung, and liver were extracted and weighted to evaluate cardiac hypertrophy and pulmonary and hepatic congestion. Heart homogenates were prepared to quantify lipid peroxidation (LPO); the activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR); and Cu-Zn SOD and GST concentrations. Total glutathione (GSH) myocardial content was also measured. Arterial pressure (142 +/- 17 mmHg) and cardiac hypertrophy index (3.4 +/- 0.45 mg/g) were significantly increased (by 38% and 22%, respectively, p<0.0001) in the aortic-banded group. LPO was enhanced by 55% in the aortic-banded group (11891 +/- 766 cps/mg protein, p<0.001) compared with that in the controls. SOD activity and concentration were higher (40% and 38%, 15.15 +/- 1.03 U/mg protein, 49.187 pixels, respectively, p<0.05) in the aortic-banded group than in the controls. Aortic-banding induced a decrease by 28% in GST (48 +/- 10 pmol/min/mg protein, p<0.005), by 36% in GPx (38.2 +/- 9.5 nmol/min/mg protein, p<0.005), by 31% in GR activities (1.55 +/- 0.23 nmol/mg protein, p<0.0005), and by 43% in GSH content (0.13 +/- 0.02 nmol/mg protein, p<0.005). In conclusion, in this model it was observed that myocardial oxidative stress induces alterations in antioxidant enzyme activities and protein expression. The follow up of these parameters could afford an early therapeutical window to avoid heart failure progression.
authors.affiliation: Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Maria H V M
authors.initials: MH
authors.lastname: Jacob
authors.forename: Mauro R N
authors.initials: MR
authors.lastname: Pontes
authors.forename: Alex S R
authors.initials: AS
authors.lastname: Araújo
authors.forename: Jaqueline
authors.initials: J
authors.lastname: Barp
authors.forename: Maria C
authors.initials: MC
authors.lastname: Irigoyen
authors.forename: Susana F
authors.initials: SF
authors.lastname: Llesuy
authors.forename: Maria F M
authors.initials: MF
authors.lastname: Ribeiro
authors.forename: Adriane
authors.initials: A
authors.lastname: Belló-Klein
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001011:Aorta / Q000473:pathology / Q000601:surgery; D006332:Cardiomegaly / Q000201:enzymology* / Q000473:pathology; D004195:Disease Models, Animal; D015971:Gene Expression Regulation, Enzymologic; D006333:Heart Failure / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control; D015227:Lipid Peroxidation; D008099:Liver / Q000201:enzymology / Q000473:pathology; D008168:Lung / Q000201:enzymology / Q000473:pathology; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants