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Quantum based effects of therapeutic nuclear magnetic resonance persistently reduce glycolysis.
Thöni, Viktoria; Mauracher, David; Ramalingam, Anil; Fiechtner, Birgit; Sandbichler, Adolf Michael; Egg, Margit.
Afiliación
  • Thöni V; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
  • Mauracher D; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
  • Ramalingam A; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
  • Fiechtner B; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
  • Sandbichler AM; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
  • Egg M; Institute of Zoology, University Innsbruck, Innsbruck, Tyrol A-6020, Austria.
iScience ; 25(12): 105536, 2022 Dec 22.
Article en En | MEDLINE | ID: mdl-36444297
ABSTRACT
Electromagnetic fields are known to induce the clock protein cryptochrome to modulate intracellular reactive oxygen species (ROS) via the quantum based radical pair mechanism (RPM) in mammalian cells. Recently, therapeutic Nuclear Magnetic Resonance (tNMR) was shown to alter protein levels of the circadian clock associated Hypoxia Inducible Factor-1α (HIF-1α) in a nonlinear dose response relationship. Using synchronized NIH3T3 cells, we show that tNMR under normoxia and hypoxia persistently modifies cellular metabolism. After normoxic tNMR treatment, glycolysis is reduced, as are lactate production, extracellular acidification rate, the ratio of ADP/ATP and cytosolic ROS, whereas mitochondrial and extracellular ROS, as well as cellular proliferation are increased. Remarkably, these effects are even more pronounced after hypoxic tNMR treatment, driving cellular metabolism to a reduced glycolysis while mitochondrial respiration is kept constant even during reoxygenation. Hence, we propose tNMR as a potential therapeutic tool in ischemia driven diseases like inflammation, infarct, stroke and cancer.
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Texto completo: 1 Base de datos: MEDLINE Idioma: En Revista: IScience Año: 2022 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Idioma: En Revista: IScience Año: 2022 Tipo del documento: Article