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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/probl11838</article-id><article-id custom-type="elpub" pub-id-type="custom">problendo-11838</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>Апоптоз роль в развитии сахарного диабета типа</article-title><trans-title-group xml:lang="en"><trans-title>Apoptosis a role in the development of type 1 diabetes</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>Мохорт</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Mokhort</surname><given-names>T. V.</given-names></name></name-alternatives><email xlink:type="simple">probl@endojournals.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>Мельнов</surname><given-names>С. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Melnov</surname><given-names>S. B.</given-names></name></name-alternatives><email xlink:type="simple">probl@endojournals.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>Горанов</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Goranov</surname><given-names>V. A.</given-names></name></name-alternatives><email xlink:type="simple">probl@endojournals.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>&lt;p&gt;Научно-исследовательский клинический институт радиационной медицины и эндокринологии&lt;/p&gt;</institution><country>Беларусь</country></aff><aff xml:lang="en"><institution>&lt;p&gt;Research Clinical Institute of Radiation Medicine and Endocrinology&lt;/p&gt;</institution><country>Belarus</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2000</year></pub-date><pub-date pub-type="epub"><day>15</day><month>04</month><year>2000</year></pub-date><volume>46</volume><issue>2</issue><issue-title>ТОМ 46, №2 (2000)</issue-title><fpage>8</fpage><lpage>13</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Мохорт Т.В., Мельнов С.Б., Горанов В.А., 2000</copyright-statement><copyright-year>2000</copyright-year><copyright-holder xml:lang="ru">Мохорт Т.В., Мельнов С.Б., Горанов В.А.</copyright-holder><copyright-holder xml:lang="en">Mokhort T.V., Melnov S.B., Goranov V.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/11838">https://www.probl-endojournals.ru/jour/article/view/11838</self-uri><abstract><p>В последние десятилетия внимание биологов и врачей разных специальностей привлекает явление апоптоза — генетически запрограммированного процесса гибели и утилизации прекоммитирован ных клеток при участии биохимических реакций, находящихся под контролем целостного организма [6|. Этот процесс запускается в результате взаимодействия регуляторных систем организма и(или) непосредственного контакта с биологически активными веществами, прямо или косвенно влияющими на функциональное состояние клеток [<xref ref-type="bibr" rid="cit2">2</xref>]. Очевидно, что апоптоз имеет огромное значение для процессов, обеспечивающих физиологическое обновление тканей в организме, и для патологических процессов, в частности аутоиммунных, сопровождающихся гибелью клеток. В настоящее время имеется достаточно оснований утверждать, что инсулинзависимый сахарный диабет (ИЗСД) возникает как следствие гибели Р-клеток (БК) в результате цитотоксического воздействия иммунологических агентов и(или) некоторых химических веществ [1 ], протекающего с участием апоптоза.</p></abstract><trans-abstract xml:lang="en"><p>In recent decades, the attention of biologists and doctors of various specialties has been attracted by the phenomenon of apoptosis a genetically programmed process of death and utilization of committed cells with the participation of biochemical reactions controlled by the whole organism [6 |. This process starts as a result of the interaction of the regulatory systems of the body and (or) direct contact with biologically active substances that directly or indirectly affect the functional state of the cells [<xref ref-type="bibr" rid="cit2">2</xref>]. Obviously, apoptosis is of great importance for the processes that ensure the physiological renewal of tissues in the body, and for pathological processes, in particular autoimmune, accompanied by cell death. At present, there is sufficient reason to assert that insulin-dependent diabetes mellitus (IDDM) occurs as a result of the death of P-cells (CD) as a result of the cytotoxic effect of immunological agents and (or) certain chemicals [<xref ref-type="bibr" rid="cit1">1</xref>] that proceeds with the participation of apoptosis.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>апоптоз</kwd><kwd>сахарный диабет</kwd><kwd>функциональное состояние клеток</kwd></kwd-group><kwd-group xml:lang="en"><kwd>apoptosis</kwd><kwd>diabetes</kwd><kwd>functional state of cells</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">Балаболкин М. И. 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