title: Increased resistance to hydrogen peroxide-induced cardiac contracture is associated with decreased myocardial oxidative stress in hypothyroid rats.
abstract: The purpose of this study was to determine whether decreased oxidative stress would increase the resistance to cardiac contracture induced by H(2)O(2) 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 H(2)O(2) (1 mmol/L), being divided into two sub-groups: control, hypothyroid, control + H(2)O(2), hypothyroid + H(2)O(2). 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 H(2)O(2)-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 H(2)O(2) challenge and is associated with decreased oxidative myocardial damage.
authors.affiliation: Physiology Department, Basic Health Sciences Institute at Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
authors.forename: Alex Sander
authors.initials: AS
authors.lastname: da Rosa Araujo
authors.forename: Madalena Freitas
authors.initials: MF
authors.lastname: Silva de Miranda
authors.forename: Ubirajara Oliveira
authors.initials: UO
authors.lastname: de Oliveira
authors.forename: Tânia
authors.initials: T
authors.lastname: Fernandes
authors.forename: Susana
authors.initials: S
authors.lastname: Llesuy
authors.forename: Luiz Carlos
authors.initials: LC
authors.lastname: Rios Kucharski
authors.forename: Neelam
authors.initials: N
authors.lastname: Khaper
authors.forename: Adriane
authors.initials: A
authors.lastname: Belló-Klein
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D003286:Contracture / Q000139:chemically induced / Q000378:metabolism*; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D007037:Hypothyroidism / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase