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

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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	da Rosa Araujo, Alex Sander Silva de Miranda, Madalena Freitas de Oliveira, Ubirajara Oliveira Fernandes, Tânia Llesuy, Susana Rios Kucharski, Luiz Carlos Khaper, Neelam Belló-Klein, Adriane
Description	Country affiliation: Brazil Author Affiliation: da Rosa Araujo AS ( Physiology Department, Basic Health Sciences Institute at Federal University of Rio Grande do Sul, Porto Alegre, Brazil.)
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. Copyright © 2009 John Wiley & Sons, Ltd.
File Format	HTM / HTML
ISSN	02636484
Issue Number	1
Volume Number	28
e-ISSN	10990844
Journal	Cell Biochemistry and Function
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-01-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Cell Biology Discipline Biochemistry Contracture Metabolism Hydrogen Peroxide Pharmacology Hypothyroidism Myocardium Oxidative Stress Drug Effects Animals Catalase Chemically Induced Disease Models, Animal Glutathione Peroxidase Lipid Peroxidation Male Protein Carbonylation Rats Rats, Wistar Superoxide Dismutase Thiobarbituric Acid Reactive Substances Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Clinical Biochemistry

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