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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">vestib</journal-id><journal-title-group><journal-title xml:lang="ru">Известия Национальной  академии наук Беларуси. Серия биологических наук</journal-title><trans-title-group xml:lang="en"><trans-title>Proceedings of the National Academy of Sciences of Belarus, Biological Series</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1029-8940</issn><issn pub-type="epub">2524-230X</issn><publisher><publisher-name>The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">vestib-175</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>Статьи</subject></subj-group></article-categories><title-group><article-title>Ингибирование функциональной активности митохондрий печени крыс при ее токсическом поражении тетрахлорметаном</article-title><trans-title-group xml:lang="en"><trans-title>Inhibition of functional activity of rat liver mitochondria under acute intoxication by carbon tetrachloride</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>Заводник</surname><given-names>И. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Zavodnik</surname><given-names>I. B.</given-names></name></name-alternatives><email xlink:type="simple">zavodnik_il@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Гродненский государственный университет имени Янки Купалы</institution></aff><aff xml:lang="en"><institution>Yanka Kupala Grodno State University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>07</day><month>06</month><year>2016</year></pub-date><volume>0</volume><issue>4</issue><fpage>104</fpage><lpage>110</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Заводник И.Б., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Заводник И.Б.</copyright-holder><copyright-holder xml:lang="en">Zavodnik I.B.</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://vestibio.belnauka.by/jour/article/view/175">https://vestibio.belnauka.by/jour/article/view/175</self-uri><abstract><p>, активность глутатионпероксидазы митохондрий, содержание оксида азота в плазме крови.</p></abstract><trans-abstract xml:lang="en"><p>Acute carbon tetrachloride-induced rat liver damage (4 g/kg) after 24 h was accompanied by a significant reduction in succinate- and glutamate-dependent mitochondrial respiration rate in state 3 (by 65 %, and by 50 %, respectively). The acceptor control ratio and respiration control ratio approached to 1, reflecting the loss of respiration control. The mitochondrial alterations were associated with oxidation of intramitochondrial GSH, the inhibition of succinate dehydrogenase (complex II) and the rise of blood plasma nitric oxide level. Melatonin administration under CCl4-induced intoxication (three times at doses of 10 mg/kg) did not cause a pronounced recovery of mitochondrial functional activity, but prevented an increase in nitric oxide level in the blood plasma of intoxicated animals and enhanced the rate of succinate oxidation in state 3 by 30 % (p &lt; 0.05).</p></trans-abstract><kwd-group xml:lang="ru"><kwd>митохондрии</kwd><kwd>интоксикация</kwd><kwd>печень</kwd><kwd>мелатонин</kwd><kwd>тетрахлорметан</kwd><kwd>потребление кислорода</kwd><kwd>оксид азота</kwd><kwd>mitochondria</kwd><kwd>intoxication</kwd><kwd>liver</kwd><kwd>melatonin</kwd><kwd>carbon tetrachloride</kwd><kwd>respiration</kwd><kwd>nitric oxide</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">Duchen, M. R. Mitochondria in health and disease: perspectives on a new mitochondrial biology / M. R. Duchen // Mol. 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