Increased resistance to hydrogen peroxide-induced cardiac contracture is associated with decreased myocardial oxidative stress in hypothyroid rats

Authors
Araujo, Alex Sander Da Rosa; Miranda, Madalena Freitas Silva de; Oliveira, Ubirajara de; Fernandes, Tânia; Llesuy, Susana Francisca; Kucharski, Luiz Carlos Rios; Khaper, Neelam; Belló Klein, Adriane
Publication Year
2010
Language
English
Format
article
Status
Published version
Description
The purpose of this study was to determine whether decreased oxidative stress would increase the resistance to cardiac contracture induced by H 2O2 in hypothyroid rats. Male Wistar rats were divided into two groups: control and hypothyroid. Hypothyroidism was induced via thyroidectomy. Four weeks post surgery, blood samples were collected to perform thyroid hormone assessments, and excised hearts were perfused at a constant flow with or without H2O2 (1 mmol/L), being divided into two sub-groups: control, hypothyroid, control + H2O2, hypothyroid + H2O2. Lipid peroxidation (LPO) was evaluated by chemiluminescence (CL) and thiobarbituric acid reactive substances (TBARS) methods, and protein oxidation by carbonyls assay in heart homogenates. Cardiac tissue was also screened for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and for total radical-trapping antioxidant potential (TRAP). Analyses of SOD and glutathione-S-transferase (GST) protein expression were also performed in heart homogenates. Hypothyroid hearts were found to be more resistant to H2O2-induced contracture (60% elevation in LVEDP) as compared to control. CL, TBARS, carbonyl, as well as SOD, CAT, GPx activities and TRAP levels were reduced (35, 30, 40, 30, 16, 25, and 33%, respectively) in the cardiac homogenates of the hypothyroid group as compared to controls. A decrease in SOD and GST protein levels by 20 and 16%, respectively, was also observed in the hypothyroid group. These results suggest that a hypometabolic state caused by thyroid hormone deficiency can lead to an improved response to H2O2 challenge and is associated with decreased oxidative myocardial damage.
Fil: Araujo, Alex Sander Da Rosa. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Miranda, Madalena Freitas Silva de. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Oliveira, Ubirajara de. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Fernandes, Tânia. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
Fil: Kucharski, Luiz Carlos Rios. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Khaper, Neelam. Lakehead University; Canadá
Fil: Belló Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil
Subject
ANTIOXIDANT ENZYMES
HEART FUNCTION
OXIDATIVE DAMAGE
PROTEIN EXPRESSION
THYROID HORMONES
Salud Ocupacional
Ciencias de la Salud
CIENCIAS MÉDICAS Y DE LA SALUD
Access level
Restricted access
License
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repository
CONICET Digital (CONICET)
Institution
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identifier
oai:ri.conicet.gov.ar:11336/67677