How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation

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How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation. / Speijer, D; Manjeri, G R; Szklarczyk, R.

In: Royal Society of London. Philosophical Transactions B. Biological Sciences, Vol. 369, No. 1646, 20130446, 05.07.2014.

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@article{8fe970b80ddf41b8a81c42897e928875,
title = "How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation",
abstract = "Oxygen radical formation in mitochondria is an incompletely understood attribute of eukaryotic cells. Recently, a kinetic model was proposed, in which the ratio between electrons entering the respiratory chain via FADH2 or NADH determines radical formation. During glucose breakdown, the ratio is low; during fatty acid breakdown, the ratio is high (the ratio increasing--asymptotically--with fatty acid length to 0.5, when compared with 0.2 for glucose). Thus, fatty acid oxidation would generate higher levels of radical formation. As a result, breakdown of fatty acids, performed without generation of extra FADH2 in mitochondria, could be beneficial for the cell, especially in the case of long and very long chained ones. This possibly has been a major factor in the evolution of peroxisomes. Increased radical formation, as proposed by the model, can also shed light on the lack of neuronal fatty acid oxidation and tells us about hurdles during early eukaryotic evolution. We specifically focus on extending and discussing the model in light of recent publications and findings.",
keywords = "Electron Transport, Fatty Acids, Humans, Mitochondria, Neurodegenerative Diseases, Oxidation-Reduction, Peroxisomes, Reactive Oxygen Species, radical formation, FADH2/NADH ratio, complex I, supercomplex, neurodegenerative disorder, peroxisome",
author = "D Speijer and Manjeri, {G R} and R Szklarczyk",
note = "{\textcopyright} 2014 The Author(s) Published by the Royal Society. All rights reserved.",
year = "2014",
month = jul,
day = "5",
doi = "10.1098/rstb.2013.0446",
language = "English",
volume = "369",
journal = "Royal Society of London. Proceedings B. Biological Sciences",
issn = "0962-8452",
publisher = "The Royal Society",
number = "1646",

}

RIS

TY - JOUR

T1 - How to deal with oxygen radicals stemming from mitochondrial fatty acid oxidation

AU - Speijer, D

AU - Manjeri, G R

AU - Szklarczyk, R

N1 - © 2014 The Author(s) Published by the Royal Society. All rights reserved.

PY - 2014/7/5

Y1 - 2014/7/5

N2 - Oxygen radical formation in mitochondria is an incompletely understood attribute of eukaryotic cells. Recently, a kinetic model was proposed, in which the ratio between electrons entering the respiratory chain via FADH2 or NADH determines radical formation. During glucose breakdown, the ratio is low; during fatty acid breakdown, the ratio is high (the ratio increasing--asymptotically--with fatty acid length to 0.5, when compared with 0.2 for glucose). Thus, fatty acid oxidation would generate higher levels of radical formation. As a result, breakdown of fatty acids, performed without generation of extra FADH2 in mitochondria, could be beneficial for the cell, especially in the case of long and very long chained ones. This possibly has been a major factor in the evolution of peroxisomes. Increased radical formation, as proposed by the model, can also shed light on the lack of neuronal fatty acid oxidation and tells us about hurdles during early eukaryotic evolution. We specifically focus on extending and discussing the model in light of recent publications and findings.

AB - Oxygen radical formation in mitochondria is an incompletely understood attribute of eukaryotic cells. Recently, a kinetic model was proposed, in which the ratio between electrons entering the respiratory chain via FADH2 or NADH determines radical formation. During glucose breakdown, the ratio is low; during fatty acid breakdown, the ratio is high (the ratio increasing--asymptotically--with fatty acid length to 0.5, when compared with 0.2 for glucose). Thus, fatty acid oxidation would generate higher levels of radical formation. As a result, breakdown of fatty acids, performed without generation of extra FADH2 in mitochondria, could be beneficial for the cell, especially in the case of long and very long chained ones. This possibly has been a major factor in the evolution of peroxisomes. Increased radical formation, as proposed by the model, can also shed light on the lack of neuronal fatty acid oxidation and tells us about hurdles during early eukaryotic evolution. We specifically focus on extending and discussing the model in light of recent publications and findings.

KW - Electron Transport

KW - Fatty Acids

KW - Humans

KW - Mitochondria

KW - Neurodegenerative Diseases

KW - Oxidation-Reduction

KW - Peroxisomes

KW - Reactive Oxygen Species

KW - radical formation

KW - FADH2/NADH ratio

KW - complex I

KW - supercomplex

KW - neurodegenerative disorder

KW - peroxisome

U2 - 10.1098/rstb.2013.0446

DO - 10.1098/rstb.2013.0446

M3 - Article

C2 - 24864314

VL - 369

JO - Royal Society of London. Proceedings B. Biological Sciences

JF - Royal Society of London. Proceedings B. Biological Sciences

SN - 0962-8452

IS - 1646

M1 - 20130446

ER -