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 <front>
  <journal-meta>
   <journal-id journal-id-type="publisher-id">Russian Journal of Biological Physics and Chemisrty</journal-id>
   <journal-title-group>
    <journal-title xml:lang="en">Russian Journal of Biological Physics and Chemisrty</journal-title>
    <trans-title-group xml:lang="ru">
     <trans-title>АКТУАЛЬНЫЕ ВОПРОСЫ БИОЛОГИЧЕСКОЙ ФИЗИКИ И ХИМИИ</trans-title>
    </trans-title-group>
   </journal-title-group>
   <issn publication-format="print">2499-9962</issn>
  </journal-meta>
  <article-meta>
   <article-id pub-id-type="publisher-id">54414</article-id>
   <article-categories>
    <subj-group subj-group-type="toc-heading" xml:lang="ru">
     <subject>Общая биофизика</subject>
    </subj-group>
    <subj-group subj-group-type="toc-heading" xml:lang="en">
     <subject>General biophysics</subject>
    </subj-group>
    <subj-group>
     <subject>Общая биофизика</subject>
    </subj-group>
   </article-categories>
   <title-group>
    <article-title xml:lang="en">ON MOLECULAR MECHANISMS OF THE EFFEECT OF MAGNETIC CONDITIONS (ZERO AND COMBINED MAGNETIC FIELDS) ON THE PRODUCTION OF REACTIVE OXYGEN SPECIES IN NEUTROPHILS</article-title>
    <trans-title-group xml:lang="ru">
     <trans-title>К ВОПРОСУ О МОЛЕКУЛЯРНЫХ МЕХАНИЗМАХ ДЕЙСТВИЯ МАГНИТНЫХ УСЛОВИЙ (НУЛЕВЫЕ И КОМБИНИРОВАННЫЕ МАГНИТНЫЕ ПОЛЯ) НА ПРОДУКЦИЮ АКТИВНЫХ ФОРМ КИСЛОРОДА В НЕЙТРОФИЛАХ</trans-title>
    </trans-title-group>
   </title-group>
   <contrib-group content-type="authors">
    <contrib contrib-type="author">
     <name-alternatives>
      <name xml:lang="ru">
       <surname>Новиков</surname>
       <given-names>В В</given-names>
      </name>
      <name xml:lang="en">
       <surname>Novikov</surname>
       <given-names>V V</given-names>
      </name>
     </name-alternatives>
     <email>docmag@mail.ru</email>
     <xref ref-type="aff" rid="aff-1"/>
    </contrib>
    <contrib contrib-type="author">
     <name-alternatives>
      <name xml:lang="ru">
       <surname>Яблокова</surname>
       <given-names>Е В</given-names>
      </name>
      <name xml:lang="en">
       <surname>Yablokova</surname>
       <given-names>E V</given-names>
      </name>
     </name-alternatives>
     <xref ref-type="aff" rid="aff-2"/>
    </contrib>
    <contrib contrib-type="author">
     <name-alternatives>
      <name xml:lang="ru">
       <surname>Фесенко</surname>
       <given-names>Е. Е.</given-names>
      </name>
      <name xml:lang="en">
       <surname>Fesenko</surname>
       <given-names>E. E.</given-names>
      </name>
     </name-alternatives>
     <xref ref-type="aff" rid="aff-3"/>
    </contrib>
   </contrib-group>
   <aff-alternatives id="aff-1">
    <aff>
     <institution xml:lang="ru">Институт биофизики клетки РАН - обособленное подразделение ФГБУН «ФИЦ «Пущинский научный центр биологических исследований РАН»</institution>
     <country>ru</country>
    </aff>
    <aff>
     <institution xml:lang="en">Institute of Cell Biophysics RAS</institution>
     <country>ru</country>
    </aff>
   </aff-alternatives>
   <aff-alternatives id="aff-2">
    <aff>
     <institution xml:lang="ru">Институт биофизики клетки РАН - обособленное подразделение ФГБУН «ФИЦ «Пущинский научный центр биологических исследований РАН»</institution>
     <country>ru</country>
    </aff>
    <aff>
     <institution xml:lang="en">Institute of Cell Biophysics RAS</institution>
     <country>ru</country>
    </aff>
   </aff-alternatives>
   <aff-alternatives id="aff-3">
    <aff>
     <institution xml:lang="ru">ФИЦ ПНЦБИ РАН</institution>
     <city>Пущино</city>
     <country>Россия</country>
    </aff>
    <aff>
     <institution xml:lang="en">PSCBR RAS</institution>
     <city>Pushchino</city>
     <country>Russian Federation</country>
    </aff>
   </aff-alternatives>
   <pub-date publication-format="print" date-type="pub" iso-8601-date="2019-06-25T20:22:29+03:00">
    <day>25</day>
    <month>06</month>
    <year>2019</year>
   </pub-date>
   <pub-date publication-format="electronic" date-type="pub" iso-8601-date="2019-06-25T20:22:29+03:00">
    <day>25</day>
    <month>06</month>
    <year>2019</year>
   </pub-date>
   <volume>4</volume>
   <issue>2</issue>
   <fpage>160</fpage>
   <lpage>167</lpage>
   <history>
    <date date-type="received" iso-8601-date="2019-06-20T20:22:29+03:00">
     <day>20</day>
     <month>06</month>
     <year>2019</year>
    </date>
    <date date-type="accepted" iso-8601-date="2019-06-20T20:22:29+03:00">
     <day>20</day>
     <month>06</month>
     <year>2019</year>
    </date>
   </history>
   <self-uri xlink:href="https://rusjbpc.ru/en/nauka/article/54414/view">https://rusjbpc.ru/en/nauka/article/54414/view</self-uri>
   <abstract xml:lang="ru">
    <p>Показано, что снижение интенсивности процессов окисления 2,7- дихлордигидрофлуоресцеина в нейтрофилах в гипомагнитных условиях не зависит от кальций-опосредованных регуляторных механизмов, о чем свидетельствует отсутствие действия внутриклеточного хелатора ионов кальция (ацетоксиметилового эфира 1,2-бис (2-аминофенокси) этан- N,N,N´, N´-тетрауксусной кислоты) на интенсивность этого процесса. Это снижение вряд ли обусловлено влиянием гипомагнитных условий на фосфорилирование компонентов НАДФН-окидазы, так как добавка ингибитора протеинкиназы С (Ro 31-6233) практически не отразилась на интенсивности флуоресценции внутриклеточного дихлордигидрофлуоресцеина. Добавка ингибитора фосфолипазы С (U73122) немного и приблизительно одинаково снизила продукцию АФК как в контроле, так и в опыте. Апоцинин в разных концентрациях вызывал рост продукции АФК в неактивированных нейтрофилах, приблизительно в два раза менее выраженный в гипомагнитных условиях. Об участии электрон-транспортной цепи митохондрий в механизме эффекта «нулевого» поля свидетельствует снижение продукции АФК при добавке ротенона, значительно более выраженное в опытных образцах. Все это резко отличает эффект «нулевого» поля от эффектов комбинированных магнитных полей, в основе которых обнаруживается влияние на регуляторные кальций-зависимые механизмы, контролирующие респираторный взрыв в нейтрофилах.</p>
   </abstract>
   <trans-abstract xml:lang="en">
    <p>It has been shown that the decrease in intensity of 2,7-dichlorodihydrofluorescein oxidation processes in neurophils under hypomagnetic field exposure is not related to the calcium-mediated mechanisms as evidenced by the absence of the effect of cell-permeant Ca2+ chelators such as 1,2-bis-(2-amino-phenoxy)ethane- N,N,N',N'-tetraacetic acid acetoxymethyl ester on the intensity of the process alluded. This decrease is hardly caused by effects of exposure to hypomagnetic field on phosphorylation of NADPH-oxidase components because addition of a protein kinase C inhibitor, Ro 31-6233, did not virtually decrease the fluorescence intensity of intracellular dichlorodihydrofluorescein. Addition of a phospholipase C inhibitor, U73122, led to a negligible decrease in ROS production in control (almost same extent as in the experiment). In the presence of apocynin at different concentrations ROS production in unactivated neutrophils increased and it was 2 time lower under hypomagnetic field conditions. A decrease in ROS production which was more apparent during the experiment after addition of rotenone is indicative of the fact that the mitochondrial electron-transport chain is involved in the mechanism of the effect of a “zero” magnetic field. All this sharply distinguishes the effect of the “zero” field from the effects of combined magnetic fields, which are based on the effect on the calcium-dependent regulatory mechanisms that control the respiratory burst in neutrophils.</p>
   </trans-abstract>
   <kwd-group xml:lang="ru">
    <kwd>гипомагнитные условия</kwd>
    <kwd>комбинированные магнитные поля</kwd>
    <kwd>флуоресценция</kwd>
    <kwd>хемилюминесценция</kwd>
    <kwd>активные формы кислорода</kwd>
    <kwd>нейтрофилы</kwd>
   </kwd-group>
   <kwd-group xml:lang="en">
    <kwd>hypomagnetic conditions</kwd>
    <kwd>combined magnetic fields</kwd>
    <kwd>fluorescence</kwd>
    <kwd>chemiluminescence</kwd>
    <kwd>reactive oxygen species</kwd>
    <kwd>neutrophils</kwd>
   </kwd-group>
  </article-meta>
 </front>
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  <p></p>
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