Induction of oxidative stress in lymphoid tissue from murine models of hypothyroidism: treatment with propylthiouracil versus thyroidectomy

ROMEO H.; KLECHA A.; CREMASCHI G.; BARREIRO ARCOS M.L.

Buenos Aires

Congreso; Reunión de Sociedades de Biociencias 2020; 2020

Sociedad Argentina de Investigación Clínica (SAIC)- Sociedad Argentina de Inmunología (SAI)- Sociedad Argentina de Fisiología (SAFIS)

Introduction: Hypothyroidism induced by antithyroid drugs increases reactive oxygen species (ROS). Some authors attribute the increase in ROS to a decrease in the intracellular concentration of non-enzymatic antioxidants and other authors to a cytotoxic effect of the drug in the liver. Objective: 1-Analyze whether the increase in ROS is a pathological condition induced by hypothyroidism or is due to the direct action of antithyroid drugs; 2-Evaluate the effect of hypothyroidism on lymphocyte functionality. Methods: Hypothyroidism was induced in Balb/c mice by treatment with propylthiouracil (PTU; 0.5g/l drinking water for 15 days) or thyroidectomy. Thyroid hormone levels were quantified by RIA. ROS were evaluated by DCFH-DA staining and flow cytometry. Liver damage was evaluated in sections of tissue stained with hematoxylin-eosin and Masson's Trichome. The number of lymphoid follicles was determined in sections of lymph nodes or spleen stained with hematoxylin-eosin. Apoptosis of lymphoid cells was quantified by flow cytometry and cell proliferation was evaluated by incorporation of [3H]-thymidine into DNA. Results: We found that both, hypothyroid mice by treatment with PTU and thyroidectomized (Thy) had an increased production of ROS in lymph nodes (LN) and spleen (S) compared to euthyroid mice (LN [MFI]: Eu-89803±10253, PTU-151393±18771, Thy-145695±15339 p