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The role of oxidation-reduction mechanisms in pathogenesis of thyroid orbitopathy
1
Studenckie Koło Naukowe przy Zakładzie Patofizjologii Katedry Patofizjologii i Endokrynologii, Wydział Lekarski z Oddziałem Lekarsko-Dentystycznym w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach
2
Zakład Patofizjologii, Wydział Lekarski z Oddziałem Lekarsko-Dentystycznym w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach
Corresponding author
Olga Dorota Łach
Zakład Patofizjologii, Wydział Lekarski z Oddziałem Lekarsko-Dentystycznym w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach, pl. Traugutta 2, 41-800 Zabrze
Zakład Patofizjologii, Wydział Lekarski z Oddziałem Lekarsko-Dentystycznym w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach, pl. Traugutta 2, 41-800 Zabrze
Ann. Acad. Med. Siles. 2019;73:150–153
KEYWORDS
TOPICS
ABSTRACT
Oxygen in the human body functions as a transmitter regulating cell bioenergetics and as a substrate in oxidation-reduction reactions, contributing to the formation of highly reactive oxygen species (ROS). The body’s antioxidant defense mechanisms include enzymatic and non-enzymatic systems. Graves’ disease, the underlying cause of which is the autoimmune process, is the most common cause of hyperthyroidism. The most common of the non-thyroid symptoms is orbital tissue inflammation called thyroid orbitopathy (TO). Under physiological conditions, there is a balance between the production of ROS and antioxidant activity. Disruption of this balance may lead to the development of oxidative stress. The article presents a review of the literature on oxidative-reduction processes in TO.
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