Schoenfeld 2016 J Cereb Blood Flow Metab: Difference between revisions
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{{Publication | {{Publication | ||
|title=SchΓΆnfeld P, Reiser G (2016) Inhibition of b-oxidation is not a valid therapeutic tool for reducing oxidative stress in conditions of neurodegeneration. J Cereb Blood Flow Metab | |title=SchΓΆnfeld P, Reiser G (2016) Inhibition of b-oxidation is not a valid therapeutic tool for reducing oxidative stress in conditions of neurodegeneration. J Cereb Blood Flow Metab 37:848-54. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/27055779 PMID: 27055779] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/27055779 PMID: 27055779] | ||
|authors=Schoenfeld P, Reiser G | |authors=Schoenfeld P, Reiser G | ||
| Line 20: | Line 20: | ||
|topics=Fatty acid | |topics=Fatty acid | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
| | |pathways=F, Other combinations | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2016-07 | |additional=2016-07 | ||
}} | }} | ||
Latest revision as of 16:23, 9 May 2017
| SchΓΆnfeld P, Reiser G (2016) Inhibition of b-oxidation is not a valid therapeutic tool for reducing oxidative stress in conditions of neurodegeneration. J Cereb Blood Flow Metab 37:848-54. |
Schoenfeld P, Reiser G (2016) J Cereb Blood Flow Metab
Abstract: According to recent reports, systemic treatment of rats with methylpalmoxirate (carnitine palmitoyltransferase-1 inhibitor) decreased peroxidation of polyunsaturated fatty acids in brain tissue. This was taken as evidence of mitochondrial Ξ²-oxidation in brain, thereby contradicting long-standing paradigms of cerebral metabolism, which claim that Ξ²-oxidation of activated fatty acids has minor importance for brain energy homeostasis. We addressed this controversy. Our experiments are the first direct experimental analysis of this question. We fueled isolated brain mitochondria or rat brain astrocytes with octanoic acid, but octanoic acid does not enhance formation of reactive oxygen species, neither in isolated brain mitochondria nor in astrocytes, even at limited hydrogen delivery to mitochondria. Thus, octanoic acid or l-octanoylcarnitine does not stimulate H2O2 release from brain mitochondria fueled with malate, in contrast to liver mitochondria (2.25-fold rise). This does obviously not support the possible occurrence of Ξ²-oxidation of the fatty acid octanoate in the brain. We conclude that a proposed inhibition of Ξ²-oxidation does not seem to be a helpful strategy for therapies aiming at lowering oxidative stress in cerebral tissue. This question is important, since oxidative stress is the cause of neurodegeneration in numerous neurodegenerative or inflammatory disease situations.
Β© The Author(s) 2016. β’ Keywords: Mitochondria, Energy metabolism, Inflammation, Lipids, Neuroprotection, Amplex red
β’ O2k-Network Lab: DE Magdeburg Schoenfeld P
Labels: MiParea: Respiration
Pathology: Neurodegenerative
Stress:Oxidative stress;RONS
Organism: Rat
Tissue;cell: Nervous system
Preparation: Isolated mitochondria
Regulation: Fatty acid Coupling state: OXPHOS Pathway: F, Other combinations HRR: Oxygraph-2k
2016-07
