Selenium Supplementation May Decrease Thyroid Peroxidase Antibody Titer via Reducing Oxidative Stress in Euthyroid Patients with Autoimmune Thyroiditis.

Xun Tian,Rui Su,Ruiguo Zhang,Chenyang Dai,Ning Li

doi:10.1155/2020/9210572

Abstract

Objective Selenium, as an antioxidant, has been implicated in the development of autoimmune thyroiditis (AIT). Many studies showed selenium supplementation could decrease thyroid autoantibodies in patients with AIT. However, the underlying mechanisms have not been well determined. Therefore, we performed a clinical study to investigate the possible mechanism of beneficial effects of selenium treatment on AIT patients. Methods Forty euthyroid patients with AIT were randomized into two groups. Group I was treated with 200 μg/day selenium supplementation, and group II received a placebo over a 3-month period. Thyroid stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb), antithyroglobulin antibody (TgAb), malondialdehyde (MDA), total antioxidant capacity (TAC), and superoxide dismutase (SOD) were measured before and 3 months after treatments. Additionally, twenty healthy volunteers also served as a control group for the evaluation of such parameters in basic condition. Results Totally, 32 patients (group I, n = 18; group II, n = 14) completed the clinical study and were incorporated into the statistics. MDA level was higher and SOD activity and TAC were lower in patients compared to healthy individuals. After 3 months, TPOAb titer significantly decreased within group I (P < 0.001) but did not change within group II (P=0.001). There were also no statistically significant changes in TSH and TgAb titers within the two groups (all P > 0.05). Additionally, decreased MDA level (from 6.8 ± 1.3 nmol/ml to 4.9 ± 0.7 nmol/ml; P < 0.001) and increased TAC (from 10.0 ± 1.9 mmol/l to 12.9 ± 3.1 mmol/l; P=0.003) and SOD activity (from 72.3 ± 10.3 U/ml to 84.3 ± 13.2 U/ml; P=0.007) were simultaneously observed after 3 months' selenium treatment. Moreover, there was a negative correlation between TAC and TgAb/TPOAb and a positive correlation between MDA and TgAb/TPOAb in AIT patients. Conclusions Our findings support the hypothesis that selenium treatment could decrease TPOAb titer via enforcing the defense against oxidative stress in euthyroid patients with AIT, which may be a potential underlying mechanism.

Highlights

Autoimmune thyroiditis (AIT) is a chronic autoimmune inflammatory disease of the thyroid gland. e T and B lymphocytes contribute to the pathogenesis of AIT by the production of autoantibodies to thyroglobulin and thyroid peroxidase and excessive reactive oxygen species (ROS) under the environmental influence or thyroid dysfunction [1]
We demonstrated that the MDA level was higher, while antioxidative defense capacity was lower in euthyroid patients with AIT as compared to healthy individuals
We found that thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) correlated positively with MDA and negatively with total antioxidant capacity (TAC), suggesting an interdependent relationship between thyroid autoimmunity and enhanced oxidative stress in AIT patients

Summary

Introduction

Autoimmune thyroiditis (AIT) is a chronic autoimmune inflammatory disease of the thyroid gland. e T and B lymphocytes contribute to the pathogenesis of AIT by the production of autoantibodies to thyroglobulin and thyroid peroxidase and excessive reactive oxygen species (ROS) under the environmental influence or thyroid dysfunction [1]. E T and B lymphocytes contribute to the pathogenesis of AIT by the production of autoantibodies to thyroglobulin and thyroid peroxidase and excessive reactive oxygen species (ROS) under the environmental influence or thyroid dysfunction [1]. Oxidative stress is defined as an imbalance between the production of ROS and antioxidant defenses. Excessive oxidative stress could cause damage to human proteins, lipids, and nucleic acids [2]. Several studies have shown increased oxidative status and decreased antioxidant defense capacity in AIT patients compared to healthy individuals [1, 3,4,5,6], whereas most of them do not focus on or ignore the impacts of thyroid dysfunction on the oxidative stress

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Conclusion