Enzymatic mechanisms of biological magnetic sensitivity.

Autor: Letuta UG; Orenburg State University, Orenburg, Russia., Berdinskiy VL; Orenburg State University, Orenburg, Russia., Udagawa C; Osaka Ohtani University, Tondabayashi, Japan., Tanimoto Y; Osaka Ohtani University, Tondabayashi, Japan.
Jazyk: angličtina
Zdroj: Bioelectromagnetics [Bioelectromagnetics] 2017 Oct; Vol. 38 (7), pp. 511-521. Date of Electronic Publication: 2017 Jul 17.
DOI: 10.1002/bem.22071
Abstrakt: Primary biological magnetoreceptors in living organisms is one of the main research problems in magnetobiology. Intracellular enzymatic reactions accompanied by electron transfer have been shown to be receptors of magnetic fields, and spin-dependent ion-radical processes can be a universal mechanism of biological magnetosensitivity. Magnetic interactions in intermediate ion-radical pairs, such as Zeeman and hyperfine (HFI) interactions, in accordance with proposed strict quantum mechanical theory, can determine magnetic-field dependencies of reactions that produce biologically important molecules needed for cell growth. Hyperfine interactions of electrons with nuclear magnetic moments of magnetic isotopes can explain the most important part of biomagnetic sensitivities in a weak magnetic field comparable to the Earth's magnetic field. The theoretical results mean that magnetic-field dependencies of enzymatic reaction rates in a weak magnetic field that can be independent of HFI constant a, if H << a, and are determined by the rate constant of chemical transformations in the enzyme active site. Both Zeeman and HFI interactions predict strong magnetic-field dependence in weak magnetic fields and magnetic-field independence of enzymatic reaction rate constants in strong magnetic fields. The theoretical results can explain the magnetic sensitivity of E. coli cell and demonstrate that intracellular enzymatic reactions are primary magnetoreceptors in living organisms. Bioelectromagnetics. 38:511-521, 2017. © 2017 Wiley Periodicals, Inc.
(© 2017 Wiley Periodicals, Inc.)
Databáze: MEDLINE