Current issue
About the Journal
Scientific Council
Editorial Board
Regulatory and archival policy
Code of publishing ethics
Publisher
Information about the processing of personal data in relation to cookies and newsletter subscription
Archive
For Authors
For Reviewers
Contact
Reviewers
Annals reviewers in 2022
Annals reviewers in 2021
Annals reviewers in 2020
Annals reviewers in 2019
Annals reviewers in 2018
Annals reviewers in 2017
Annals reviewers in 2016
Annals reviewers in 2015
Annals reviewers in 2014
Annals reviewers in 2013
Annals reviewers in 2012
Links
Sklep Wydawnictwa SUM
Biblioteka Główna SUM
Śląski Uniwersytet Medyczny w Katowicach
Privacy policy
Accessibility statement
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.
REFERENCES (31)
1.
Haddad J.J. Antioxidant and prooxidant mechanisms in the regulation of redox(y)-sensitive transcription factors. Cell. Signal. 2002; 14(11): 879–897, doi: 10.1016/S0898-6568(02)00053-0.
2.
Zerrouki M., Benkaci-Ali F. DFT study of the mechanisms of nonenzymatic DNA repair by phytophenolic antioxidants. J. Mol. Model. 2018; 24(4): 78, doi: 10.1007/s00894-018-3599-6.
3.
Haddad J.J. Oxygen sensing and oxidant/redox-related pathways. Biochem. Biophys. Res. Commun. 2004; 316(4): 969–977, doi: 10.1016/j. bbrc.2004.02.162.
4.
Puzanowska-Tarasiewicz H., Starczewska B., Kuźmicka L. Reaktywne formy tlenu. Bromat. Chem. Toksykol. 2008; 41(4): 1007–1015.
5.
Key T.J., Allen N.E., Spencer E.A., Travis R.C. The effect of diet on risk of cancer. Lancet 2002; 360(9336): 861–868, doi: 10.1016/S0140-6736(02)09958-0.
6.
Karihtala P., Soini Y. Reactive oxygen species and antioxidant mechanisms in human tissues and their relation to malignancies. APMIS 2007; 115(2): 81–103, doi: 10.1111/j.1600-0463.2007.apm_514.x.
7.
Valko M., Leibfritz D., Moncol J., Cronin M.T., Mazur M., Telser J. Free radicals and antioxidants in normal physiological functions and human disease. Int. J. Biochem. Cell Biol. 2007; 39(1): 44–84, doi: 10.1016/j.biocel.2006.07.001.
8.
Karpińska A., Gromadzka G. Stres oksydacyjny i naturalne mechanizmy antyoksydacyjne – znaczenie w procesie neurodegeneracji. Od mechanizmów molekularnych do strategii terapeutycznych. Postepy Hig. Med. Dosw. 2013; 67: 43–53.
9.
Guz J., Dziaman T., Szpila A. Czy witaminy antyoksydacyjne mają wpływ na proces karcynogenezy? Postepy Hig. Med. Dosw. 2007: 185–198.
10.
Birkner E., Zalejska-Fiolka J., Antoszewski Z. Aktywność enzymów antyoksydacyjnych i rola witamin o charakterze antyoksydacyjnym w chorobie Alzheimera. Postepy Hig. Med. Dosw. 2004; 58: 264–269.
11.
Bartalena L. Diagnosis and management of Graves disease: a global overview. Nat. Rev. Endocrinol. 2013; 9(12): 724–734, doi:10.1038/nrendo.2013.193.
12.
Menconi F., Marcocci C., Marinò M. Diagnosis and classification of Graves’ disease. Autoimmun. Rev. 2014; 13(4–5): 398–402, doi: 10.1016/j.autrev.2014.01.013.
13.
Smith T.J., Hegedüs L. Graves’ Disease. N. Engl. J. Med. 2016; 375(16): 1552–1565, doi: 10.1056/NEJMra1510030.
14.
Bartley G.B., Fatourechi V., Kadrmas E.F., Jacobsen S.J., Ilstrup D.M., Garrity J.A., Gorman C.A. The Incidence of Graves’ Ophthalmopathy in Olmsted County, Minnesota. Am. J. Ophthalmol. 1995: 120(4): 511–517.
15.
Hondur A., Konuk O., Dincel A.S., Bilgihan A., Unal M., Hasanreisoglu B. Oxidative stress and antioxidant activity in orbital fibroadipose tissue in Graves’ ophthalmopathy. Curr. Eye Res. 2008; 33(5–6): 421–427, doi:10.1080/02713680802123532.
16.
Venditti P., Di Meo S. Thyroid hormone-induced oxidative stress. Cell. Mol. Life Sci. 2006; 63(4): 414–434, doi:10.1007/s00018-005-5457-9.
17.
Khong J.J., McNab A.A., Ebeling P.R., Craig J.E., Selva D. Pathogenesis of thyroid eye disease: Review and update on molecular mechanisms. Br. J. Ophthalmol. 2016; 100(1): 142–150, doi: 10.1136/bjophthalmol-2015-307399.
18.
Rotondo Dottore G., Leo M., Casini G., Latrofa F., Cestari L., Sellari-Franceschini S., Nardi M., Vitti P., Marcocci C., Marinò M. Antioxidant Actions of Selenium in Orbital Fibroblasts: A Basis for the Effects of Selenium in Graves’ Orbitopathy. Thyroid 2017; 27(2): 271–278, doi: 10.1089/thy.2016.0397.
19.
Marcocci C., Kahaly G.J., Krassas G.E., Bartalena L., Prummel M., Stahl M., Altea M.A., Nardi M., Pitz S., Boboridis K., Sivelli P. et al. Selenium and the Course of Mild Graves’ Orbitopathy. N. Engl. J. Med. 2011; 364(20): 1920–1931, doi: 10.1056/NEJMoa1012985.
20.
Tsai C.C., Cheng C.Y., Liu C.Y., Kao S.C., Kau H.C., Hsu W.M., Wei Y.H. Oxidative stress in patients with Graves’ ophthalmopathy: Relationship between oxidative DNA damage and clinical evolution. Eye 2009; 23(8): 1725–1730, doi: 10.1038/eye.2008.310.
21.
Tsai C.C., Kao S.C., Cheng C.Y., Kau H.C., Hsu W.M., Lee C.F., Wei Y.H. Oxidative Stress Change by Systemic Corticosteroid Treatment Among Patients Having Active Graves Ophthalmopathy. Arch. Ophthalmol. 2007; 125(12): 1652–1656.
22.
Bartalena L., Piantanida E. Cigarette smoking: Number one enemy for Graves ophthalmopathy. Pol. Arch. Med. Wewn. 2016; 126(10): 725–726, doi: 10.20452/pamw.3592.
23.
Tellez M., Cooper J., Edmonds C. Graves’ ophthalmopathy in relation to cigarette smoking and ethnic origin. Clin. Endocrinol. 1992; 36(3): 291–294, doi:10.1111/j.1365-2265.1992.tb01445.x.
24.
Yoon J.S., Lee H.J., Chae M.K., Lee S.Y., Lee E.J. Cigarette smoke extract-induced adipogenesis in Graves’ orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress. J. Endocrinol. 2013; 216(2): 145–156, doi: 10.1530/JOE-12-0257.
25.
Cawood T.J., Moriarty P., O’Farrelly C., O’Shea D. Smoking and thyroid-associated ophthalmopathy: A novel explanation of the biological link. J. Clin. Endocrinol. Metab. 2007; 92(1): 59–64, doi: 10.1210/jc.2006-1824.
26.
Bednarek J., Wysocki H., Sowiński J. Oxidative stress peripheral parameters in Graves’ disease: The effect of methimazole treatment in patients with and without infiltrative ophthalmopathy. Clin. Biochem. 2005; 38(1): 13–18, doi: 10.1016/j.clinbiochem.2004.09.015.
27.
Burch H.B., Lahiri S., Bahn R.S., Barnes S. Superoxide radical production stimulates retroocular fibroblast proliferation in graves’ ophthalmopathy. Exp. Eye Res. 1997; 65(2): 311–316, doi: 10.1006/exer.1997.0353.
28.
Tsai C.C., Wu S.B., Kao S.C., Kau H.C., Lee F.L., Wei Y.H. The protective effect of antioxidants on orbital fibroblasts from patients with Graves’ ophthalmopathy in response to oxidative stress. Mol. Vis. 2013; 19: 927–934.
29.
Lindquist S. The heat-shock response. Ann. Rev. Biochem. 1986; 55: 1151–1191.
30.
Heufelder A.E., Wenzel B.E., Bahn R.S. Methimazole and Propylthiouracil Inhibit the Oxygen Free Radical-Induced Expression of a 72 Kilodalton Shock Protein in Graves’ Retrooculat Fibroblasts. J. Clin. Endocrinol. Metab. 1992; 74(4): 737–742.
31.
Heufelder A.E., Wenzel B.E., Bahn R.S. Cell surface localization of a 72 kilodalton heat shock protein in retroocular fibroblasts from patients with Graves’ ophthalmopathy. J. Clin. Endocrinol. Metab. 1992; 74(4): 732–736.
RELATED ARTICLE
The Medical University of Silesia in Katowice, as the Operator of the annales.sum.edu.pl website, processes personal data collected when visiting the website. The function of obtaining information about Users and their behavior is carried out by voluntarily entered information in forms, saving cookies in end devices, as well as by collecting web server logs, which are in the possession of the website Operator. Data, including cookies, are used to provide services in accordance with the Privacy policy.
You can consent to the processing of data for these purposes, refuse consent or access more detailed information.
You can consent to the processing of data for these purposes, refuse consent or access more detailed information.