Measurement of Oxygen Radicals and Lipid Peroxidation in Neural Tissues

Hall, Edward D.; Bosken, Jeffrey M.

doi:10.1002/0471142301.ns0717s11

Cited by 16 publications

(17 citation statements)

References 29 publications

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“…Lipid peroxidates are unstable indicators of oxidative stress in neurons [44]. 4-hydroxy-2-nonenol (HNE) is the final product of lipid peroxidation.…”

Section: Methodsmentioning

confidence: 99%

Reduced VDAC1 Protects Against Alzheimer's Disease, Mitochondria, and Synaptic Deficiencies

Mańczak

Sheiko

Craigen

et al. 2013

JAD

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The objective of this study was to elucidate the effect of VDAC1 on Alzheimer’s disease (AD)-related genes, mitochondrial activity, and synaptic viability. Recent knockout studies of VDAC1 revealed that homozygote VDAC1 knockout (VDAC1−/−) mice exhibited disrupted learning and synaptic plasticity, and in contrast, VDAC1+/− mice appeared normal in terms of lifespan, fertility, and viability relative to wild-type mice. However, the effects of reduced VDAC1 on mitochondrial/synaptic genes and mitochondrial function in AD-affected neurons are not well understood. In the present study, we characterized mitochondrial/synaptic and AD-related genes and mitochondrial function in VDAC1+/− mice and VDAC1+/+ mice. We found reduced mRNA levels in the AD-related genes, including AβPP, Tau, PS1, PS2, and BACE1; increased levels of the mitochondrial fusion genes Mfn1, Mfn2; reduced levels of the fission genes Drp1 and Fis1; and reduced levels of the mitochondrial permeability transition pore genes VDAC1, ANT, and CypD in VDAC1+/− mice relative to VDAC1+/+ mice. Hexokinase 1 and 2 were significantly upregulated in the VDAC+/− mice. The synaptic genes synaptophysin, synapsin 1 and 2, synaptobrevin 1 and 2, neurogranin, and PSD95 were also upregulated in the VDAC1+/− mice. Free radical production and lipid peroxidation levels were reduced in the VDAC1+/− mice, and cytochrome oxidase activity and ATP levels were elevated, indicating enhanced mitochondrial function in the VDAC1+/− mice. These findings suggest that reduced VDAC1 expression, such as that we found in the VDAC1+/− mice, may be beneficial to synaptic activity, may improve function, and may protect against toxicities of AD-related genes.

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“…Lipid peroxidates are unstable indicators of oxidative stress in neurons [44]. 4-hydroxy-2-nonenol (HNE) is the final product of lipid peroxidation.…”

Section: Methodsmentioning

confidence: 99%

Reduced VDAC1 Protects Against Alzheimer's Disease, Mitochondria, and Synaptic Deficiencies

Mańczak

Sheiko

Craigen

et al. 2013

JAD

View full text Add to dashboard Cite

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“…Lipid peroxidates are unstable indicators of oxidative stress in neurons [30]. 4-hydroxy-2-nonenol (HNE) is the final product of lipid peroxidation that was measured in cerebral cortex and cerebellum tissues of Drp1+/− mice (n=3) and Drp1+/+ mice (n=3), with an HNE-His ELISA Kit (Cell BioLabs, Inc., San Diego, CA).…”

Section: Mitochondrial Functionmentioning

confidence: 99%

Dynamin-related protein 1 heterozygote knockout mice do not have synaptic and mitochondrial deficiencies

Mańczak

Sesaki

Kageyama

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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The objective of this study was to elucidate the effect of partial reduction of the mitochondrial fission protein, dynamin-related protein 1 (Drp1) on mitochondrial activity and synaptic viability. Recent knockout studies of Drp1 revealed that homozygote Drp1 knockout mice are embryonic lethal due to reduced mitochondrial fission, and that this reduced fission leads to developmental defects in the brain. In contrast, heterozygote Drp1 knockout mice appear to be normal in terms of lifespan, fertility, and viability, and phenotypically these animals are not different from wild-type mice. However, the effects of partial Drp1 reduction on mitochondrial function and synaptic activity are not well understood. In the present study, we sought to characterize synaptic, dendritic and mitochondrial proteins, and mitochondrial function and GTPase enzymatic activity, in Drp1 heterozygote knockout mice. Interestingly, we found no significant changes in synaptic, dendritic, and mitochondrial proteins in the Drp1 heterozygote knockout mice compared to the wild-type mice. Further, mitochondrial function and GTPase enzymatic activity appeared to be normal. However, H2O2 and lipid peroxidation levels were significantly reduced in the Drp1 heterozygote knockout mice compared to the wild-type mice. These findings suggest that partial Drp1 reduction does not affect mitochondrial and synaptic viability and may have therapeutic use in treating patients with Alzheimer’s disease and Huntington’s disease.

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“…Neurons have a physiologically higher level of oxidative stress than nonnerve cells (Maher and Schubert 2000;Hall and Andrus 2001). This higher stress level may create a state of diminished anti-oxidative reserve capacity and contribute to their negative response to ROS mediators.…”

Section: Possible Mechanisms Of Inhibition Of Cntf and Ifn-cmentioning

confidence: 99%

“…Nerve cells have a greatly increased oxidative metabolic load compared with other cells resulting in greater potential for oxidative stress (Maher and Schubert 2000;Hall and Andrus 2001). The increased oxidative metabolism is derived from a variety of sources including catecholamine oxidation, 5-lipoxygenase, nitric oxide synthase, microglia and mitochondrial damage (Hall and Andrus 2001;Dröge 2002). The mediators of oxidative stress, e.g.…”

mentioning

confidence: 99%

Inducers of oxidative stress block ciliary neurotrophic factor activation of Jak/STAT signaling in neurons

Kaur¹,

Lu²,

Ward³

et al. 2005

Journal of Neurochemistry

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Generation of reactive oxygen species (ROS) with the accumulation of oxidative damage has been implicated in neurodegenerative disease and in the degradation of nervous system function with age. Here we report that ROS inhibit the activity of ciliary neurotrophic factor (CNTF) in nerve cells. Treatment with hydrogen peroxide (H 2 O 2 ) as a generator of ROS inhibited CNTF-mediated Jak/STAT signaling in all cultured nerve cells tested, including chick ciliary ganglion neurons, chick neural retina, HMN-1 motor neuron hybrid cells, and SH-SY5Y and BE(2)-C human neuroblastoma cells. H 2 O 2 treatment of non-neuronal cells, chick skeletal muscle and HepG2 hepatoma cells, did not inhibit Jak/STAT signaling. The H 2 O 2 block of CNTF activity was seen at concentrations as low as 0.1 mM and within 15 min, and was reversible upon removal of H 2 O 2 from the medium. Also, two other mediators of oxidative stress, nitric oxide and rotenone, inhibited CNTF signaling. Treatment of neurons with H 2 O 2 and rotenone also inhibited interferon-c-mediated activation of Jak/STAT1. Depleting the intracellular stores of reduced glutathione by treatment of BE(2)-C cells with nitrofurantoin inhibited CNTF activity, whereas addition of reduced glutathione protected cells from the effects of H 2 O 2 . These results suggest that disruption of neurotrophic factor signaling by mediators of oxidative stress may contribute to the neuronal damage observed in neurodegenerative diseases and significantly affect the utility of CNTF-like factors as therapeutic agents in preventing nerve cell death. Keywords: ciliary neurotrophic factor, cytokine, gpl30, reactive oxygen species, signal transduction, tyrosine kinase. Signaling through the ciliary neurotrophic factor (CNTF) receptor has been implicated in the development, survival and maintenance of a broad range of neurons and glia in the PNS and CNS, as well as cardiac and skeletal muscle. CNTF receptors are essential for embryonic development and the receptor knockout phenotype in mice is embryonic lethal (DeChiara et al. 1995). Defects in CNTF expression result in an impaired neural injury response in mice (Masu et al. 1993;Yao et al. 1999;Linker et al. 2002) and decreased neuron numbers in embryonic chick (Ernsberger et al. 1989;Finn et al. 1998). In addition, a variety of neuronal, glial and muscle cell types show responses to CNTF in vivo or in vitro affecting neuronal phenotype, neurotransmitter receptor levels, neurotransmitter release, metabolism and survival (Adler et al.

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Measurement of Oxygen Radicals and Lipid Peroxidation in Neural Tissues

Cited by 16 publications

References 29 publications

Reduced VDAC1 Protects Against Alzheimer's Disease, Mitochondria, and Synaptic Deficiencies

Reduced VDAC1 Protects Against Alzheimer's Disease, Mitochondria, and Synaptic Deficiencies

Dynamin-related protein 1 heterozygote knockout mice do not have synaptic and mitochondrial deficiencies

Inducers of oxidative stress block ciliary neurotrophic factor activation of Jak/STAT signaling in neurons

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