Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balbc Mice
Joint Authors
Barreiro Arcos, María L.
Costilla, Melisa
Macri Delbono, Rodrigo
Klecha, Alicia
Cremaschi, Graciela Alicia
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-06-02
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Costilla, Melisa& Macri Delbono, Rodrigo& Klecha, Alicia& Cremaschi, Graciela Alicia& Barreiro Arcos, María L.. 2019. Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balbc Mice. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205160
Modern Language Association (MLA)
Costilla, Melisa…[et al.]. Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balbc Mice. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1205160
American Medical Association (AMA)
Costilla, Melisa& Macri Delbono, Rodrigo& Klecha, Alicia& Cremaschi, Graciela Alicia& Barreiro Arcos, María L.. Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balbc Mice. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1205160
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205160