Oxidative stress activates insulin-like growth factor I receptor protein expression, mediating cardiac hypertrophy induced by thyroxine |
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Authors: | A S R Araujo A T Enzveiler P Schenkel T R G Fernandes M F M Ribeiro W A Partata S Llesuy A Belló-Klein |
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Institution: | (1) Departamento Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, 90050-170 Porto Alegre, RS, Brazil;(2) Cátedra de Química General y Inorgánica, Facultad de Farmácia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina;(3) Departamento de Fisiologia e Farmacologia, Universidade Federal de Santa Maria, Santa Maria, Brazil |
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Abstract: | Thyroxine can cause cardiac hypertrophy by activating growth factors, such as IGF-I (insulin-like growth factor-I). Since
oxidative stress is enhanced in the hyperthyroidism, it would control protein expression involved in this hypertrophy. Male
Wistar rats were divided into four groups: (I) control, (II) vitamin E-supplemented (20 mg/kg/day subcutaneous), (III) hyperthyroid
(thyroxine 12 mg/l, in drinking water), and (IV) hyperthyroid + vitamin E. After 4 weeks, the contractility and relaxation
indexes of left ventricle (LV), and cardiac mass were increased by 54%, 60%, and 60%, respectively, in hyperthyroid group.
An increase in lipid peroxidation (around 40%), and a decrease in total glutathione (by 20%) was induced by thyroxine and
avoided by vitamin E administration. Superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were increased
(by 83% and 54%, respectively) in hyperthyroid, and vitamin E avoided changes in SOD. Protein expression of SOD, GST, and
IGF-I receptor (IGF-IR) were increased (by 87%, 84%, and 60%, respectively) by thyroxine, and vitamin E promoted a significant
reduction in SOD and IGF-IR expression (by 36% and 17%, respectively). These results indicate that oxidative stress is involved
in cardiac hypertrophy, and suggest a role for IGF-IR as a mediator of this adaptive response in experimental hyperthyroidism. |
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Keywords: | Hyperthyroidism Glutathione metabolism Heart failure Protein expression Vitamin E IGF-IR |
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