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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">akusherstvo</journal-id><journal-title-group><journal-title xml:lang="en">Obstetrics, Gynecology and Reproduction</journal-title><trans-title-group xml:lang="ru"><trans-title>Акушерство, Гинекология и Репродукция</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2313-7347</issn><issn pub-type="epub">2500-3194</issn><publisher><publisher-name>IRBIS LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.17749/2070-4968.2015.9.4.055-065</article-id><article-id custom-type="elpub" pub-id-type="custom">akusherstvo-182</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="en"><subject>REVIEW ARTICLE</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>НАУЧНЫЙ ОБЗОР</subject></subj-group></article-categories><title-group><article-title>MITOCHONDRIAL DYSFUNCTION AS POSSIBLE CAUSE OF IMPAIRED FOLLICULAR DEVELOPMENT</article-title><trans-title-group xml:lang="ru"><trans-title>МИТОХОНДРИАЛЬНАЯ ДИСФУНКЦИЯ КАК ОДНА ИЗ ВОЗМОЖНЫХ ПРИЧИН НАРУШЕНИЯ ФОЛЛИКУЛО- И СТЕРОИДОГЕНЕЗА ПРИ ПРЕЖДЕВРЕМЕННОЙ НЕДОСТАТОЧНОСТИ ЯИЧНИКОВ</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Позднякова</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Pozdnyakova</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант отделения гинекологической эндокринологии</p></bio><bio xml:lang="en"><p>the graduate student of office of gynecologic endocrinology</p></bio><email xlink:type="simple">anna_pozd@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Володина</surname><given-names>М. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Volodina</surname><given-names>M. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.б.н., н.с. лаборатории митохондриальной медицины</p></bio><bio xml:lang="en"><p>PhD, researcher at mitochondrial medicine research group</p></bio><email xlink:type="simple">m_volodina@oparina4.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рштуни</surname><given-names>С. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Rshtuni</surname><given-names>S. J.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант отделения гинекологической эндокринологии</p></bio><bio xml:lang="en"><p>the graduate student of office of gynecologic endocrinology</p></bio><email xlink:type="simple">rshtunisandra@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Марченко</surname><given-names>Л. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Marchenko</surname><given-names>L. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, ведущий научный сотрудник отделения гинекологической эндокринологии</p></bio><bio xml:lang="en"><p>the doctor of medical sciences, the professor, the leading researcher</p></bio><email xlink:type="simple">l.a.marchenko@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Высоких</surname><given-names>М. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Vysokikh</surname><given-names>M. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.б.н., зав. лабораторией митохондриальной медицины</p></bio><bio xml:lang="en"><p>PhD, Head of mitochondrial medicine research group</p></bio><email xlink:type="simple">m_vysokikh@oparina4.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ «Научный центр акушерства, гинекологии и перинатологии им. академика В.И. Кулакова» Минздрава России, Москва</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Center for Obstetrics, Gynecology and Perinatology of the Ministry of Healthcare of the Russian Federation</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБУ «Научный центр акушерства, гинекологии и перинатологии им. академика В.И. Кулакова» Минздрава России, Москва, Подразделение МГУ «Научно-исследовательский институт физико-химической биологии&#13;
им. А.Н. Белозерского», Москва</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Center for Obstetrics, Gynecology and Perinatology of the Ministry of Healthcare of the Russian Federation, Subdivision of Moscow State University "Scientific Research Institute of Physico-Chemical Biology named after AN Belozersky", Moscow</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>20</day><month>06</month><year>2016</year></pub-date><volume>9</volume><issue>4</issue><fpage>55</fpage><lpage>65</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Pozdnyakova A.A., Volodina M.A., Rshtuni S.J., Marchenko L.A., Vysokikh M.Y., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Позднякова А.А., Володина М.А., Рштуни С.Д., Марченко Л.А., Высоких М.Ю.</copyright-holder><copyright-holder xml:lang="en">Pozdnyakova A.A., Volodina M.A., Rshtuni S.J., Marchenko L.A., Vysokikh M.Y.</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.gynecology.su/jour/article/view/182">https://www.gynecology.su/jour/article/view/182</self-uri><abstract><p>Mitochondria play leading role in senescence program realization. One of the early manifestations of this process is loss of reproductive function in female (menopause). In this review we discuss up-to-date data on basic mitochondria functions and their possible role in development of premature ovarian insufficienсy and morbid conditions associated with this state, that are typical for ageing organism. Besides performing function of conversion of free energy by cell respiration substrates oxidation mitochondria control survival and death of somatic cells and gametes maintaining optimal level of reactive oxygen species in cells. Oxidative stress results in selective death of specialized cells; organs and tissues functionality disturbance; leads to development of cardiovascular, locomotor and nervous disorders. The main reason of oxidative stress is mitochondrial disfunction induced by disbalance between reactive oxygen species production and their utilization by antioxidant system. On the other hand mitochondria play central role in intracellular signal transmission and maintain functional state and cellular structure of tissues, organs and systems of an organism controlling cell proliferation, differentiation and apoptosis. Finally mitochondria define largely immune response in case of infections and tumoral transformation and control sex hormones level taking part in steroidogenesis. It was found that high level of damaged mitochondrial DNA, decrease of its copy number and increase of reactive oxygen species production in ovarian tissue cells are typical for women suffering from premature ovarian insufficienсy. Chronic oxidative stress leads not only to oogenesis disturbance and decrease of oocyte maturation probability but promotes also cardiovascular diseases, osteoporosis and other delayed consequences of estrogen deficit development in case of this state.</p></abstract><trans-abstract xml:lang="ru"><p>Митохондрии играют ведущую роль в реализации программы старения организма, одним из ранних проявлений которого является выключение репродуктивной функции у женщин (менопауза). В представленном обзоре обсуждены современные данные об основных функциях митохондрий и их возможной роли в развитии преждевременной недостаточности яичников и ассоциированных с ней патологических состояний, характерных для старческого организма. Наряду с выполнением функции преобразования свободной энергии посредством окисления субстратов дыхания данные органеллы контролируют выживание и гибель как соматических, так и половых клеток за счет поддержания оптимального клеточного уровня активных форм кислорода. С одной стороны, окислительный стресс приводит к селективной гибели специализированных клеток, снижению функциональности органов и тканей, определяет развитие заболеваний сердечно-сосудистой, костной, нервной систем. Основной причиной окислительного стресса является митохондриальная дисфункция, индуцированная нарушением баланса между продукцией активных форм кислорода и их утилизацией системой антиоксидантного контроля. С другой стороны, митохондрии, являясь центральным звеном внутриклеточной передачи сигнала, поддерживают функциональное состояние и клеточный состав тканей, органов и систем организма, контролируя пролиферацию, дифференцировку и апоптоз клеток. Наконец, митохондрии во многом определяют уровень иммунного ответа организма при инфекции или опухолевой трансформации и контролируют уровень половых гормонов, участвуя в стероидогенезе. Известно, что для женщин с преждевременной недостаточностью яичников характерен повышенный уровень повреждений в митохондриальной ДНК, снижение числа ее копий и повышение уровня продукции активных форм кислорода в клетках тканей яичника. Состояние хронического окислительного стресса не только приводит к нарушениям оогенеза и снижению вероятности созревания яйцеклетки, но и способствует развитию сердечно-сосудистых заболеваний, остеопороза и других отдаленных последствий эстрогенного дефицита при данной патологии.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>Преждевременная недостаточность яичников</kwd><kwd>митохондрия</kwd><kwd>митохондриальная дисфункция</kwd><kwd>окислительный стресс</kwd><kwd>апоптоз</kwd><kwd>TSPO</kwd><kwd>p66shc</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Premature ovarian insufficienсy</kwd><kwd>mitochondria</kwd><kwd>mitochondrial disfunction</kwd><kwd>oxidative stress</kwd><kwd>apoptosis</kwd><kwd>TSPO</kwd><kwd>p66shc</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">Вейсман А. Лекции по эволюционной теории, читанные в Университете во Фрейбурге (в Брейсгау) проф. 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