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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Clinical nutrition and metabolism</journal-id><journal-title-group><journal-title xml:lang="en">Clinical nutrition and metabolism</journal-title><trans-title-group xml:lang="ru"><trans-title>Клиническое питание и метаболизм</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2658-4433</issn><issn publication-format="electronic">2782-2974</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">88951</article-id><article-id pub-id-type="doi">10.17816/clinutr88951</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Научные обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Pathophysiological aspects of oxygen, hypoxia and free radical oxidation in critical conditions</article-title><trans-title-group xml:lang="ru"><trans-title>Патофизиологические аспекты кислорода, гипоксии и свободнорадикального окисления при критических состояниях</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6747-998X</contrib-id><contrib-id contrib-id-type="spin">3811-7817</contrib-id><name-alternatives><name xml:lang="en"><surname>Orlov</surname><given-names>Yurii P.</given-names></name><name xml:lang="ru"><surname>Орлов</surname><given-names>Юрий Петрович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Dr. Sci. (Med.), Assistant Professor</p></bio><bio xml:lang="ru"><p>д.м.н., доцент</p></bio><email>orlov-up@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9976-8903</contrib-id><contrib-id contrib-id-type="spin">4974-9195</contrib-id><name-alternatives><name xml:lang="en"><surname>Sviridov</surname><given-names>Sergey V.</given-names></name><name xml:lang="ru"><surname>Свиридов</surname><given-names>Сергей Викторович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Dr. Sci. (Med.), Professor</p></bio><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><email>sviridov.ru@mail.ru</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2811-6051</contrib-id><contrib-id contrib-id-type="spin">5953-4315</contrib-id><name-alternatives><name xml:lang="en"><surname>Kakulya</surname><given-names>Evgeny N.</given-names></name><name xml:lang="ru"><surname>Какуля</surname><given-names>Евгений Николаевич</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>к.м.н., ассистент кафедры анестезиологии и реаниматологии Омского государственного медицинского университета</p>
<p> </p></bio><email>vrach2248@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Omsk State Medical University</institution></aff><aff><institution xml:lang="ru">Омский государственный медицинский университет</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">The Russian National Research Medical University named after N.I. Pirogov</institution></aff><aff><institution xml:lang="ru">Российский национальный исследовательский медицинский университет имени Н.И. Пирогова</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2021-04-15" publication-format="electronic"><day>15</day><month>04</month><year>2021</year></pub-date><volume>2</volume><issue>2</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>66</fpage><lpage>79</lpage><history><date date-type="received" iso-8601-date="2021-11-24"><day>24</day><month>11</month><year>2021</year></date><date date-type="accepted" iso-8601-date="2021-12-10"><day>10</day><month>12</month><year>2021</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2021, Orlov Y.P., Sviridov S.V., Kakulya E.N.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2021, Орлов Ю.П., Свиридов С.В., Какуля Е.Н.</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="en">Orlov Y.P., Sviridov S.V., Kakulya E.N.</copyright-holder><copyright-holder xml:lang="ru">Орлов Ю.П., Свиридов С.В., Какуля Е.Н.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://journals.eco-vector.com/2658-4433/article/view/88951">https://journals.eco-vector.com/2658-4433/article/view/88951</self-uri><abstract xml:lang="en"><p>Oxygen is the main regulator of metabolic processes in the body not only in the context of normal physiology, but also in the development of various critical conditions.</p> <p>In recent years, the problem of pathogenesis of a number organs' and systems' diseases has been enriched by knowledge of the mechanism of damage to cellular structures. Oxygen turned out to be the main factor of damage — the very oxygen, due to the lack of which cell death occurs. It turned out that the so-called reactive oxygen species having an unpaired electron have a biological effect, which, depending on the concentration, can be regulatory or, conversely, toxic. Accordingly, interest has also been aroused in compounds that normally prevent the toxic effect of reactive oxygen species — antioxidants. Today it is generally recognized that oxidative stress plays an important and possibly a key role in the pathogenesis of critical conditions. Thus, on the one side, excessive production of free radicals is considered as one of the manifestations of the body's protective reaction to the effects of various environmental factors and living conditions (infections, injuries, toxins, ionizing radiation, physical stress, hypothermia, hypoxia, various types of stress), on the other ― increased production of free radicals quickly leads to irreversible damage: destruction of the erythrocytes' membranes with subsequent hemolysis, transformation of hemoglobin into methemoglobin, DNA damage, desensitization of plasma membrane receptors, inactivation of various hormones and enzymes, including antiradical and antiperoxide protection enzymes.</p> <p>The problem of using oxygen in critical conditions is currently widely discussed in the periodical literature with an emphasis on the oxygen concentrations used in patients, both in operating rooms and in intensive care units. Oxygen used in the intensive care of acute respiratory failure and hypoxia should have a certain concentration range. The toxic effects of oxygen can occur with its prolonged use in high concentrations, which causes not only its direct toxic effect on the lungs, but also in the potentiation of the activation of free radical oxidation and excessive production of reactive oxygen species.</p> <p>The review presents current data on the physiological role of oxygen, its participation in metabolic processes against the background of inflammation, hypoxia and under conditions of activation of free radical oxidation processes. The recent approach to oxygen therapy and the research data presented in the review urge to relate to oxygen as a drug in order to avoid manifestations of its toxic effects.</p></abstract><trans-abstract xml:lang="ru"><p>Кислород является основным регулятором метаболических процессов в организме не только в контексте нормальной физиологии, но и при развитии различных критических состояний.</p> <p>В последние годы проблема патогенеза целого ряда заболеваний органов и систем обогатилась знанием механизма повреждения клеточных структур. Основным фактором повреждения оказался кислород — тот самый кислород, из-за недостатка которого возникает гибель клеток. Выяснилось, что так называемые активные формы кислорода, имеющие неспаренный электрон, обладают биологическим эффектом, который в зависимости от концентрации может быть регуляторным или, наоборот, токсическим. Соответственно, пробудился интерес и к соединениям, которые в обычных условиях предотвращают токсическое действие активных форм кислорода, — антиоксидантам. Сегодня общепризнано, что окислительный стресс играет важную, если не ключевую роль в патогенезе критических состояний. Таким образом, с одной стороны, избыточная продукция свободных радикалов рассматривается как одно из проявлений защитной реакции организма на воздействие различных факторов окружающей среды и условий жизнедеятельности (инфекции, травмы, токсины, ионизирующее излучение, физическое напряжение, переохлаждение, гипоксия, различного вида стрессы), с другой ― повышенная продукция свободных радикалов достаточно быстро приводит к необратимым повреждениям: разрушению мембран эритроцитов с последующим гемолизом, превращению гемоглобина в метгемоглобин, повреждению ДНК, десенситизации рецепторов плазматических мембран, инактивации различных гормонов и ферментов, в том числе ферментов антирадикальной и антиперекисной защиты.</p> <p>Проблема использования кислорода при критических состояниях в настоящее время широко обсуждается в периодической литературе с акцентированием внимания на его концентрациях, применяемых у пациентов как в операционных, так и в отделениях реанимации и интенсивной терапии. Кислород, используемый в процессе интенсивной терапии острой дыхательной недостаточности и гипоксии, должен иметь определённый диапазон значений концентрации. Токсические эффекты кислорода могут проявляться при его длительном использовании в высоких концентрациях, что обусловливает не только его прямой токсический эффект на лёгкие, но и активацию свободнорадикального окисления и избыточной продукции активных форм кислорода.</p> <p>В обзоре изложены современные данные о физиологической роли кислорода, его участии в процессах метаболизма на фоне воспаления, гипоксии и в условиях активации процессов свободнорадикального окисления. Современный подход к оксигенотерапии и представленные в обзоре данные исследований призывают относиться к кислороду как к лекарственному препарату во избежание проявлений его токсических эффектов.</p></trans-abstract><kwd-group xml:lang="en"><kwd>metabolism</kwd><kwd>oxygen</kwd><kwd>hypoxia</kwd><kwd>free radical oxidation</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>метаболизм</kwd><kwd>кислород</kwd><kwd>гипоксия</kwd><kwd>свободнорадикальное окисление</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">Bosco G, Paganini M, Giacon TA, et al. Oxidative stress and inflammation, MicroRNA, and hemoglobin variations after administration of oxygen at different pressures and concentrations: a randomized trial. 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