The role of advanced glycation end products and oxidative stress in the pathophysiology of thyroid disorders
The disorders of the thyroid gland have grown in increasing rates at the last decades, making the awareness of their disorders very critical worldwide. Oxidative stress plays important role in the pathophysiology of wide spectrum of disorders including thyroiditis. In this study, papillary thyroid c...
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Sprache: | eng |
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Zusammenfassung: | The disorders of the thyroid gland have grown in increasing rates at the last decades, making the awareness of their disorders very critical worldwide. Oxidative stress plays important role in the pathophysiology of wide spectrum of disorders including thyroiditis. In this study, papillary thyroid cancer (ThC), Hashimoto’s disease (HD), and Grave’s disease (GD) were considered as subjects for the investigation of advance glycation end products (AGEs) and its relationship to oxidative stress by evaluating malondialdehyde (MDA) and thiol levels. The study included 90 subjects, 62 of which were suffering from thyroid disorders (19 HD, 19 GD, and 24 ThC). Serum of each subject was analyzed for AGEs, MDA, and thiol. Serum AGEs level was increased significantly in ThC patients (1217.73±473.32 ng/mL), HD patients (791.29±329.48 ng/mL), and GD patients (829.29±348.85 ng/mL). ThC patients have shown significant higher levels of AGEs compared to HD and GD patients, while no significant differences observed between the last two groups. Moreover, MDA level was increased in all of the thyroid patients, most significantly in ThC patients which was significantly higher than GD patients, but non-significantly higher than GD patients. Thiol level was decreased significantly in ThC, HD, and GD patients with no significant differences among the patients. ThC patients have shown positive correlation between AGEs and MDA (r=0.791). Also, AGEs biomarker was excellent in the prognosis of thyroid disorders, especially ThC. Elevated levels of AGEs in thyroiditis patients can cause a shift in the redox balance by increasing the production of cellular ROS. |
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ISSN: | 0094-243X 1551-7616 |
DOI: | 10.1063/5.0235820 |