Hyperthyroidism is an endocrine condition marked by excessive thyroxine (T3) and triiodothyronine (T3) secretion (T4). Thyroid hormones (THs) have pleiotropic effects on a variety of tissues and cause an overall rise in metabolism, including higher energy demand and oxygen consumption. As a result, the aim of this study was to look into the effects of hyperthyroidism on the development of reactive oxygen species (ROS) in euthyroid and hyperthyroid mice’s lymph node and spleen cells, as well as the antioxidant mechanisms involved in resetting the cellular redox state. Thirty female Balb/c mice were randomly assigned to one of two groups: euthyroid (placebo treatment) or hyperthyroid (treatment with 12 mg/l T4 in drinking water for 30 days). In lymph node and spleen cells of hyperthyroid mice, we discovered a substantial increase in ROS as well as an increase in the genomic and protein expression of the antioxidant enzymes Catalase (CAT) and Glutathione peroxidase-1 (GPx-1). The expression of CAT and GPx-1 was increased in lymphoid cells from euthyroid mice after in vitro treatment with H2O2 (250 M). The phosphorylation levels of Nrf-2 (Nuclear Factor Erythroid 2-related factor) and the kinase activity of Protein Kinase C (PKC) and Extracellular Signal-Regulated Kinase were increased by hyperthyroidism (ERK). Furthermore, we discovered an improvement in the expression of the classic PKC isoenzymes, and. Nrf-2 was phosphorylated and translocated to the cell nucleus by the PKC and ERK kinases. In conclusion, these findings showed that a rise in ROS in hyperthyroid mice’s lymphoid tissue induced the transcription of antioxidant enzymes by activating Nrf-2. In lymphoid cells from hyperthyroid mice, we explain the molecular mechanisms that regulate the enzymatic antioxidant system. The discovery of new molecular targets for the treatment of pathologies linked to elevated levels of oxidative stress could be aided by understanding how the cellular redox state is modulated.

Author (s) Details

Melisa Costilla
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

Rodrigo Macri Delbono
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

Alicia Klecha
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

Mariana Daniela Kovalovsky-Barreiro
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

Graciela Cremaschi
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

María Laura Barreiro Arcos
Institute for Biomedical Research (BIOMED), Argentine Catholic University (UCA), National Council for Scientific and Technical Research (CONICET), Avenue Alicia Moreau de Justo 1600 (C1107AAZ), Buenos Aires, Argentina

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