Lipid peroxidation in brain or spinal cord mitochondria after injury

Edward D. Hall; Juan A. Wang; Jeffrey M. Bosken; Indrapal N. Singh

doi:10.1007/s10863-015-9600-5

Lipid peroxidation in brain or spinal cord mitochondria after injury

Edward D. Hall, Juan A. Wang, Jeffrey M. Bosken, Indrapal N. Singh

Neuroscience

Research output: Contribution to journal › Article › peer-review

105 Scopus citations

Abstract

Extensive evidence has demonstrated an important role of oxygen radical formation (i.e., oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO₂), hydroxyl radical (•OH) and carbonate radical (•CO₃). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed.

Original language	English
Pages (from-to)	169-174
Number of pages	6
Journal	Journal of Bioenergetics and Biomembranes
Volume	48
Issue number	2
DOIs	https://doi.org/10.1007/s10863-015-9600-5
State	Published - Apr 1 2016

Bibliographical note

Publisher Copyright:
© 2015, Springer Science+Business Media New York.

Funding

The research described in the authors' laboratory was partially funded by grants from the National Institute of Neurological Disorders & Stroke (NINDS) including R01 NS046566, R01 NS083405, R01 NS084857, P01 NS058484, R21 NS077434 and P30 NS051220 and grants from the Kentucky Spinal Cord & Head Injury Research Trust. The research described in the authors’ laboratory was partially funded by grants from the National Institute of Neurological Disorders & Stroke (NINDS) including R01 NS046566, R01 NS083405, R01 NS084857, P01 NS058484, R21 NS077434 and P30 NS051220 and grants from the Kentucky Spinal Cord & Head Injury Research Trust.

Funders	Funder number
National Institutes of Health (NIH)
Institute of Neurological Disorders and Stroke National Advisory Neurological Disorders and Stroke Council	R01NS083405, R01NS084857, P01 NS058484, R01 NS046566, R21NS077434, P30 NS051220
Institute of Neurological Disorders and Stroke National Advisory Neurological Disorders and Stroke Council
Kentucky Spinal Cord and Head Injury Research Trust

Keywords

Antioxidant
Lipid peroxidation
Mitochondria
Oxidative stress
Spinal cord injury
Traumatic brain injury

ASJC Scopus subject areas

Physiology
Cell Biology

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10.1007/s10863-015-9600-5

Cite this

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title = "Lipid peroxidation in brain or spinal cord mitochondria after injury",

abstract = "Extensive evidence has demonstrated an important role of oxygen radical formation (i.e., oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO2), hydroxyl radical (•OH) and carbonate radical (•CO3). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed.",

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AU - Hall, Edward D.

AU - Wang, Juan A.

AU - Bosken, Jeffrey M.

AU - Singh, Indrapal N.

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N2 - Extensive evidence has demonstrated an important role of oxygen radical formation (i.e., oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO2), hydroxyl radical (•OH) and carbonate radical (•CO3). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed.

AB - Extensive evidence has demonstrated an important role of oxygen radical formation (i.e., oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO2), hydroxyl radical (•OH) and carbonate radical (•CO3). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed.

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KW - Oxidative stress

KW - Spinal cord injury

KW - Traumatic brain injury

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Lipid peroxidation in brain or spinal cord mitochondria after injury

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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