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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">vestim</journal-id><journal-title-group><journal-title xml:lang="ru">Известия Национальной  академии наук Беларуси. Серия медицинских наук</journal-title><trans-title-group xml:lang="en"><trans-title>Proceedings of the National Academy of Sciences of Belarus, Medical series</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1814-6023</issn><issn pub-type="epub">2524-2350</issn><publisher><publisher-name>The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29235/1814-6023-2020-17-4-409-416</article-id><article-id custom-type="elpub" pub-id-type="custom">vestim-707</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>КЛИНИЧЕСКАЯ И ЭКСПЕРИМЕНТАЛЬНАЯ МЕДИЦИНА</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL AND EXPERIMENTAL MEDICINE</subject></subj-group></article-categories><title-group><article-title>Взаимодействие аргиназы и L-аргинин-NO системы печени в процессах детоксикации, развития оксидативного стресса и формирования тиреоидного статуса у крыс при хронической этаноловой интоксикации</article-title><trans-title-group xml:lang="en"><trans-title>Interaction of liver arginase and L-arginine-NO system in the processes of detoxification, lipid peroxidation and the formation of the thyroid status in rats with chronic ethanol intoxication</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>Лобанова</surname><given-names>В. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Lobanova</surname><given-names>V. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Лобанова Валерия Валерьевна – ассистент</p><p>пр. Дзержинского, 83, 220116, г. Минск</p></bio><bio xml:lang="en"><p>Valeria V. Lobanova – Assistant</p><p>83, Dzerzhinski Ave., 220116, Minsk</p></bio><email xlink:type="simple">patfiz@bsmu.by</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>Висмонт</surname><given-names>Ф. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Vismont</surname><given-names>F. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Висмонт Франтишек Иванович – член-корреспондент, доктор медицинских наук, профессор, заведующий кафедрой</p><p>пр. Дзержинского, 83, 220116, г. Минск</p></bio><bio xml:lang="en"><p>Frantishek I. Vismont – Corresponding Member, D. Sc. (Med.), Professor, Head of the Department</p><p>83, Dzerzhinski Ave., 220116, Minsk</p></bio><email xlink:type="simple">patfiz@bsmu.by</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Белорусский государственный медицинский университет</institution></aff><aff xml:lang="en"><institution>Belarusian State Medical University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>05</day><month>12</month><year>2020</year></pub-date><volume>17</volume><issue>4</issue><fpage>409</fpage><lpage>416</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Лобанова В.В., Висмонт Ф.И., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Лобанова В.В., Висмонт Ф.И.</copyright-holder><copyright-holder xml:lang="en">Lobanova V.V., Vismont F.I.</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://vestimed.belnauka.by/jour/article/view/707">https://vestimed.belnauka.by/jour/article/view/707</self-uri><abstract><p>К настоящему времени накопилось достаточное количество фактов, свидетельствующих о том, что аргиназа печени и монооксид азота играют значительную роль в процессах жизнедеятельности в норме и при патологии. Целью исследования было выяснение значимости взаимосвязи и взаимодействия аргиназы и L-аргинин-NO системы печени в процессах детоксикации, развития оксидативного стресса и формировании тиреоидного статуса у крыс при хронической этаноловой интоксикации. 2 В опытах на крысах с использованием современных физиологических, биохимических методов исследования и фармакологического подхода было установлено, что хроническая этаноловая интоксикация приводит к снижению активности аргиназы печени, концентрации трийодтиронина и к повышению уровня «средних молекул», NO3 – /NO2 – , содержания продуктов ПОЛ в плазме, степени токсичности крови, активности аланинаминотрансферразы и аспартатаминотрансферразы, продолжительности наркотического сна. У гипертиреоидных крыс повышается, а у крыс с экспериментальным гипотиреозом снижается активность аргиназы печени, процессов детоксикации, ПОЛ и температура тела. Депрессия аргиназы печени, вызываемая введением в организм Nω-гидрокси-нор-L-аргинином (Nor-NOHA), а также L-валина, препятствует повышению температуры тела и развитию характерных изменений процессов детоксикации и ПОЛ на действие экзогенного трийодтиронина. В условиях угнетения аргиназы печени как Nor-NOHA, так и L-валином действие этанола сопровождается более значимым угнетением детоксикационной функции печени и повышением содержания NO3 – /NO2 – в плазме крови. Предварительное введение в организм животным ингибитора NO-синтазы метилового эфира NG-нитро-L-аргинина ослабляет токсический эффект этанола на печень, а также развитие характерных изменений активности аргиназы печени, процессов детоксикации и ПОЛ у крыс с хронической этаноловой интоксикацией. По-видимому, от активности аргиназы и L-аргинин-NO системы печени зависит выраженность процессов детоксикации, ПОЛ и формирование тиреоидного статуса в условиях хронической алкоголизации, что играет значимую роль в патогенезе этаноловой интоксикации.</p></abstract><trans-abstract xml:lang="en"><p>A sufficient number of facts testifying the importance of liver arginase and nitrogen monoxide in the life processes in the normal and pathological conditions have been accumulated to date. The aim of the study was to determine the significance of the relationship and interaction of liver arginase and L-arginine-NO system in the processes of detoxification, lipid peroxidation and the formation of the thyroid status in rats with chronic ethanol intoxication. In rat experiments using the modern physiological, biochemical research methods and a pharmacological approach, it was found that chronic ethanol intoxication leads to a decrease in the liver arginase activity and the triiodothyronine concentration. At the same time, the increase in the level of “average molecules”, NO3 – /NO2 –, the content of lipid peroxidation products in the plasma, as well as the increase in the blood toxicity degree, the activity of alanine amino transferase, aspartate amino transferase and the narcotic sleep duration were observed. Hyperthyroid rats demonstrated the increased liver arginase activity, the processes of detoxification, lipid peroxidation and body temperature while rats with the experimental hypothyroidism showed the opposite results. The liver arginase depression caused by the injection of Nω-hydroxy-nor-L-arginine (Nor-NOHA), or L-valine into the body prevents the body temperature increase and the development of characteristic changes in the detoxification and lipid peroxidation processes acted upon by exogenous triiodothyronine. Under the conditions of the liver arginase inhibition by Nor-NOHA or L-valine, the ethanol action is accompanied by a more significant inhibition of the liver detoxification function and an increase of NO3 – /NO2 – levels in blood plasma. The preliminary injection of an NG-nitro-L-arginine methyl ester inhibitor of NO-synthase into the animal’s body weakensthe toxic ethanol effect on the liver, as well asthe development of characteristic changes in the liver arginase activity, in the processes of detoxification and lipid peroxidation in rats with chronic ethanol intoxication. Apparently, the activity of liver arginase and L-arginine-NO system determines the severity of detoxification, lipid peroxidation processes and the formation of the thyroid status in the conditions of chronic alcoholization, which is important in the ethanol intoxication pathogenesis.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая этаноловая интоксикация</kwd><kwd>детоксикация</kwd><kwd>аргиназа печени</kwd><kwd>перекисное окисление липидов</kwd><kwd>L-аргинин-NO система</kwd><kwd>крысы</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic ethanol intoxication</kwd><kwd>detoxification</kwd><kwd>liver arginase</kwd><kwd>lipid peroxidation</kwd><kwd>L-arginine-NO system</kwd><kwd>rats</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">Buko V. U., Lukivskaya O. Ya., Khokha A. M. Metabolic effects of alcohol intoxication. 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