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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">problendo</journal-id><journal-title-group><journal-title xml:lang="ru">Проблемы Эндокринологии</journal-title><trans-title-group xml:lang="en"><trans-title>Problems of Endocrinology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0375-9660</issn><issn pub-type="epub">2308-1430</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/probl11827</article-id><article-id custom-type="elpub" pub-id-type="custom">problendo-11827</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>Оксидативный стресс и его роль в развитии аутоиммунных заболеваний щитовидной железы</article-title><trans-title-group xml:lang="en"><trans-title>Oxidative stress and its role in the development of autoimmune thyroid diseases</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1248-9099</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рыбакова</surname><given-names>Анастасия Андреевна</given-names></name><name name-style="western" xml:lang="en"><surname>Rybakova</surname><given-names>Anastasia A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>научный сотрудник отдела терапевтической эндокринологии</p></bio><bio xml:lang="en"><p>MD</p></bio><email xlink:type="simple">aamamykina@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6388-1544</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Платонова</surname><given-names>Надежда Михайловна</given-names></name><name name-style="western" xml:lang="en"><surname>Platonova</surname><given-names>Nadezhda M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>доктор медицинских наук, главный научный сотрудник отдела терапевтической эндокринологи</p></bio><bio xml:lang="en"><p>MD, ScD</p></bio><email xlink:type="simple">doc-platonova@inbox.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8520-8702</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трошина</surname><given-names>Екатерина Анатольевна</given-names></name><name name-style="western" xml:lang="en"><surname>Troshina</surname><given-names>Ekaterina A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>доктор медицинских наук, профессор, член-корреспондент РАН, заместитель директора Центра по координации эндокринологической службы, руководитель Координационного совета, руководитель отдела терапевтической эндокринологии</p></bio><bio xml:lang="en"><p>MD, ScD, professor</p></bio><email xlink:type="simple">troshina@inbox.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр эндокринологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Endocrinology Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>10</day><month>06</month><year>2020</year></pub-date><volume>65</volume><issue>6</issue><fpage>451</fpage><lpage>457</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Рыбакова А.А., Платонова Н.М., Трошина Е.А., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Рыбакова А.А., Платонова Н.М., Трошина Е.А.</copyright-holder><copyright-holder xml:lang="en">Rybakova A.A., Platonova N.M., Troshina E.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.probl-endojournals.ru/jour/article/view/11827">https://www.probl-endojournals.ru/jour/article/view/11827</self-uri><abstract><p>В настоящее время известно большое количество социально значимых заболеваний, в которых тканевые повреждения сопровождаются развитием оксидативного стресса. В развитии этих заболеваний свободные радикалы играют решающую роль. Аналогичные процессы происходят под действием источников ионизирующего излучения, а также при бактериальных инфекциях. В последнее время появились научные данные, свидетельствующие о значительной роли оксидативного стресса в развитии аутоиммунных тиреопатий. Предполагается, что синтез тиреоидных гормонов зависит от концентрации Н2О2, которая из-за высокой токсичности должна находиться в строгом соответствии с активностью антиоксидантных систем. В норме, многие биохимически-неблагоприятные процессы протекают на апикальной мембране тиреоцита, что позволяет ограничить действие свободных радикалов и избежать деструкции клетки. Однако, при патологических состояниях происходит нарушение ферментативных систем и их компоненты становятся аномально активированными в цитоплазме, а это, в свою очередь, приводит к функциональным и морфологическим нарушениям. Более глубокое понимание природы оксидативного стресса и его роли в развитии АИТ может способствовать выявлению новых методов его оценки, расширению терапевтических диапазонов в отношении данного заболевания. В обзоре обсуждается оксидативный стресс, представляющий собой, накопление активных повреждающих агентов (свободных радикалов, прооксидантов, активных форм кислорода), инициирующих повреждение клеток и ведущих к развитию различных патологических состояний. Его основу составляет свободнорадикальное окисление жирных кислот, или так называемое перекисное окисление липидов.</p></abstract><trans-abstract xml:lang="en"><p>A large number of socially significant diseases is accompanied with oxidative stress and carry with tissue damage. Free radicals play a crucial role in the development of these diseases. Similar processes occur under the influence of ionizing radiation and bacterial infections. Recently, was indicated the significant role of oxidative stress in the development of autoimmune thyroiditis. It is assumed that the synthesis of thyroid hormones depends on the concentration of H2O2, which, due to its high toxicity, must be in strict accordance with the activity of antioxidant systems. Many biochemically negative processes occur on the apical membrane of the thyrocyte, which allows limiting the effect of free radicals and avoid cell destruction. However, in pathological conditions, enzymatic systems are disturbed and their components become abnormally activated in the cytoplasm, and it is leads to functional and morphological disorders. A deeper understanding of oxidative stress and its role in the development of autoimmune thyroiditis can contribute to the identification of new methods for its assessment, the expansion of therapeutic ranges for this disease. This review discusses oxidative stress, which is the accumulation of active damaging agents (free radicals, prooxidants, reactive oxygen species) that initiate cell damage and lead to the development of various pathological conditions.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>оксидативный стресс</kwd><kwd>гипотиреоз</kwd><kwd>гипертиреоз</kwd><kwd>щитовидная железа</kwd><kwd>аутоиммунность</kwd></kwd-group><kwd-group xml:lang="en"><kwd>oxidative stress</kwd><kwd>hypothyroidism</kwd><kwd>hyperthyroidism</kwd><kwd>thyroid gland</kwd><kwd>autoimmunity</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Betteridge D. What is oxidative stress? Metabol. 2000;49(2 suppl 1): 3-8. doi: https://doi.org/10.1016/s0026-0495(00)80077-3</mixed-citation><mixed-citation xml:lang="en">Betteridge D. What is oxidative stress? 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