Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8673
Título : Oxidative stress produced by hyperthyroidism status induces the antioxidant enzyme transcription through the activation of the nrf-2 factor in lymphoid tissues of balb/c mice
Autor : Costilla, Melisa 
Macri Delbono, Rodrigo 
Klecha, Alicia Juana 
Cremaschi, Graciela A. 
Barreiro Arcos, María Laura 
Palabras clave : HIPERTIROIDISMOGANGLIOS LINFATICOSESTRES OXIDATIVO
Fecha de publicación : 2019
Editorial : Hindawi
Cita : Costilla M, Macri Delbono R, Klecha A, Cremaschi GA, Barreiro Arcos ML. Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balb/c Mice [en línea]. Oxidative Medicine and Cellular Longevity 2019. doi:10.1155/2019/7471890 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8673
Resumen : Abstract: Hyperthyroidism is an endocrine disorder characterized by excessive secretion of thyroid hormones T3 and T4. Thyroid hormones exert pleiotropic actions on numerous tissues and induce an overall increase in metabolism, with an increase in energy demand and oxygen consumption. Therefore, the purpose of this study was to investigate the effects of hyperthyroidism on the production of reactive oxygen species (ROS) in lymph node and spleen cells of euthyroid and hyperthyroid mice, analyzing antioxidant mechanisms involved in the restitution of the cellular redox state. For this, thirty female Balb/c (H-2d) mice were randomly divided into two groups: euthyroid (by treatment with placebo) and hyperthyroid (by treatment with 12 mg/l of T4 in drinking water for 30 days). We found a significant increase in ROS and an increase in the genomic and protein expression of the antioxidant enzymes catalase (CAT) and glutathione peroxidase-1 (GPx-1) in lymph node and spleen cells of hyperthyroid mice. In vitro treatment with H2O2 (250 μM) of the lymphoid cells of euthyroid mice increased the expression levels of CAT and GPx-1. The hyperthyroidism increased the phosphorylation levels of Nrf2 (nuclear factor erythroid 2-related factor) and the kinase activity of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK). Additionally, we found an increase in the expression of the classic isoenzymes of PKCα, β and γ. In conclusion, these results indicated that the increase in ROS found in the hyperthyroid state induces the antioxidant enzyme transcription through the activation of the Nrf-2 factor in lymphoid tissues. This shows the influence of hyperthyroidism on the regulation of the cellular antioxidant system.
URI : https://repositorio.uca.edu.ar/handle/123456789/8673
ISSN : 1942-0900 (print)
1942-0994 (online)
Disciplina: MEDICINA
DOI: 10.1155/2019/7471890
Derechos: Acceso Abierto
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