Energy, Entropy and Quantum Tunneling of Protons and Electrons in Brain Mitochondria: Relation to Mitochondrial Impairment in Aging-Related Human Brain Diseases and Therapeutic Measures

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F21%3A00075234" target="_blank" >RIV/00159816:_____/21:00075234 - isvavai.cz</a>

Result on the web

<a href="https://www.mdpi.com/2227-9059/9/2/225/htm" target="_blank" >https://www.mdpi.com/2227-9059/9/2/225/htm</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/biomedicines9020225" target="_blank" >10.3390/biomedicines9020225</a>

Result language

angličtina

Original language name

Energy, Entropy and Quantum Tunneling of Protons and Electrons in Brain Mitochondria: Relation to Mitochondrial Impairment in Aging-Related Human Brain Diseases and Therapeutic Measures

Original language description

Adult human brains consume a disproportionate amount of energy substrates (2-3% of body weight; 20-25% of total glucose and oxygen). Adenosine triphosphate (ATP) is a universal energy currency in brains and is produced by oxidative phosphorylation (OXPHOS) using ATP synthase, a nano-rotor powered by the proton gradient generated from proton-coupled electron transfer (PCET) in the multi-complex electron transport chain (ETC). ETC catalysis rates are reduced in brains from humans with neurodegenerative diseases (NDDs). Declines of ETC function in NDDs may result from combinations of nitrative stress (NS)-oxidative stress (OS) damage; mitochondrial and/or nuclear genomic mutations of ETC/OXPHOS genes; epigenetic modifications of ETC/OXPHOS genes; or defects in importation or assembly of ETC/OXPHOS proteins or complexes, respectively; or alterations in mitochondrial dynamics (fusion, fission, mitophagy). Substantial free energy is gained by direct O-2 -mediated oxidation of NADH. Traditional ETC mechanisms require separation between O-2 and electrons flowing from NADH/FADH(2) through the ETC. Quantum tunneling of electrons and much larger protons may facilitate this separation. Neuronal death may be viewed as a local increase in entropy requiring constant energy input to avoid. The ATP requirement of the brain may partially be used for avoidance of local entropy increase. Mitochondrial therapeutics seeks to correct deficiencies in ETC and OXPHOS.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10608 - Biochemistry and molecular biology

Project

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Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2021

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

BIOMEDICINES

ISSN

2227-9059

e-ISSN

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Volume of the periodical

9

Issue of the periodical within the volume

2

Country of publishing house

CH - SWITZERLAND

Number of pages

20

Pages from-to

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UT code for WoS article

000622142300001

EID of the result in the Scopus database

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