title: Redox status and pro-survival/pro-apoptotic protein expression in the early cardiac hypertrophy induced by experimental hyperthyroidism.
abstract: This study was conducted to analyse the redox status and redox-sensitive proteins that may contribute to a non-genomic mechanism of cardiac hypertrophy induction by hyperthyroidism. Wistar rats, treated with L-thyroxine (T4) during 2 weeks (12 mg·l(-1) in drinking water), presented cardiac hypertrophy (68% higher than control), without signals of liver or lung congestion. Myocardial reduction of the reduced glutathione: oxidized glutathione (GSSG) ratio (45%) (redox status) and elevation in hydrogen peroxide concentration (H(2) O(2) ) (28%) were observed in hyperthyroid as compared with the control. No significant difference was found in thioredoxin (Trx), Trx reductase activity and Nrf2 (a transcriptional factor) protein expression between groups. Redox-sensitive proteins, quantified using Western blot, presented the following results: increased p-ERK: total extracellular-regulated kinase (ERK) (200%) and Bax:Bcl-2 (62%) ratios and reduced total-Akt (63%) and p-Akt (53%) expressions in the hyperthyroid rats as compared with the control. The redox imbalance, associated with increased immunocontent of a protein related to maladaptative growth (ERK) and reduced immunocontent of protein related to cytoprotection/survival (Akt), may suggest that the molecular scenario could favour the decompensation process of cardiac hypertrophy induced by experimental hyperthyroidism.
authors: Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
authors: R O
authors: RO
authors: Fernandes
authors: G J
authors: GJ
authors: Dreher
authors: P C
authors: PC
authors: Schenkel
authors: T R G
authors: TR
authors: Fernandes
authors: M F M
authors: MF
authors: Ribeiro
authors: A S R
authors: AS
authors: Araujo
authors: A
authors: A
authors: Belló-Klein
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D015153:Blotting, Western; D006332:Cardiomegaly / Q000139:chemically induced* / Q000473:pathology; D016923:Cell Death; D060766:Drinking Water / Q000008:administration & dosage; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D006980:Hyperthyroidism / Q000139:chemically induced* / Q000473:pathology; D020935:MAP Kinase Signaling System; D008297:Male; D023421:Models, Animal; D010084:Oxidation-Reduction; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013879:Thioredoxins / Q000378:metabolism; D013974:Thyroxine / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; C494828:Bax protein, rat; D060766:Drinking Water; D051028:bcl-2-Associated X Protein; D013879:Thioredoxins; D006861:Hydrogen Peroxide; D051057:Proto-Oncogene Proteins c-akt; D005978:Glutathione; D013974:Thyroxine; D019803:Glutathione Disulfide