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  1. AU="Doria, Margaux"
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  1. Article ; Online: Docosahexaenoic Acid Attenuates Mitochondrial Alterations and Oxidative Stress Leading to Cell Death Induced by Very Long-Chain Fatty Acids in a Mouse Oligodendrocyte Model.

    Nury, Thomas / Doria, Margaux / Lizard, Gérard / Vejux, Anne

    International journal of molecular sciences

    2020  Volume 21, Issue 2

    Abstract: In the case of neurodegenerative pathologies, the therapeutic arsenal available is often directed towards the consequences of the disease. The purpose of this study is, therefore, to evaluate the ability of docosahexaenoic acid (DHA), a molecule present ... ...

    Abstract In the case of neurodegenerative pathologies, the therapeutic arsenal available is often directed towards the consequences of the disease. The purpose of this study is, therefore, to evaluate the ability of docosahexaenoic acid (DHA), a molecule present in certain foods and considered to have health benefits, to inhibit the cytotoxic effects of very long-chain fatty acids (C24:0, C26:0), which can contribute to the development of some neurodegenerative diseases. The effect of DHA (50 µM) on very long-chain fatty acid-induced toxicity was studied by several complementary methods: phase contrast microscopy to evaluate cell viability and morphology, the MTT test to monitor the impact on mitochondrial function, propidium iodide staining to study plasma membrane integrity, and DHE staining to measure oxidative stress. A Western blot assay was used to assess autophagy through modification of LC3 protein. The various experiments were carried out on the cellular model of 158N murine oligodendrocytes. In 158N cells, our data establish that DHA is able to inhibit all tested cytotoxic effects induced by very long-chain fatty acids.
    MeSH term(s) Animals ; Cell Line ; Cell Survival/drug effects ; Docosahexaenoic Acids/pharmacology ; Fatty Acids/analysis ; Membrane Potential, Mitochondrial/drug effects ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Models, Animal ; Oligodendroglia/cytology ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism
    Chemical Substances Fatty Acids ; Reactive Oxygen Species ; Docosahexaenoic Acids (25167-62-8) ; hexacosanoic acid (D42CQN6P36)
    Language English
    Publishing date 2020-01-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21020641
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Protective function of autophagy during VLCFA-induced cytotoxicity in a neurodegenerative cell model.

    Doria, Margaux / Nury, Thomas / Delmas, Dominique / Moreau, Thibault / Lizard, Gérard / Vejux, Anne

    Free radical biology & medicine

    2019  Volume 137, Page(s) 46–58

    Abstract: In recent years, a particular interest has focused on the accumulation of fatty acids with very long chains (VLCFA) in the occurrence of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis or dementia. Indeed, it seems increasingly ...

    Abstract In recent years, a particular interest has focused on the accumulation of fatty acids with very long chains (VLCFA) in the occurrence of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis or dementia. Indeed, it seems increasingly clear that this accumulation of VLCFA in the central nervous system is accompanied by a progressive demyelination resulting in death of neuronal cells. Nevertheless, molecular mechanisms by which VLCFA result in toxicity remain unclear. This study highlights for the first time in 3 different cellular models (oligodendrocytes 158 N, primary mouse brain culture, and patient fibroblasts) the types of cell death involved where VLCFA-induced ROS production leads to autophagy. The autophagic process protects the cell from this VLCFA-induced toxicity. Thus, autophagy in addition to oxidative stress can offer new therapeutic approaches.
    MeSH term(s) Animals ; Autophagy/physiology ; Brain/pathology ; Cell Death ; Cells, Cultured ; Fatty Acids/metabolism ; Fibroblasts/physiology ; Humans ; Mice ; Mice, Inbred BALB C ; Neurodegenerative Diseases/metabolism ; Neurons/physiology ; Oligodendroglia/physiology ; Oxidative Stress ; Reactive Oxygen Species/metabolism
    Chemical Substances Fatty Acids ; Reactive Oxygen Species
    Language English
    Publishing date 2019-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2019.04.016
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    Zs.A 2109: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Contribution of cholesterol and oxysterols to the pathophysiology of Parkinson's disease.

    Doria, Margaux / Maugest, Lucie / Moreau, Thibault / Lizard, Gérard / Vejux, Anne

    Free radical biology & medicine

    2016  Volume 101, Page(s) 393–400

    Abstract: Neurodegenerative diseases are a major public health issue worldwide. Some countries, including France, have engaged in research into the causes of Parkinson's disease, Alzheimer's disease, and multiple sclerosis and the management of these patients. It ... ...

    Abstract Neurodegenerative diseases are a major public health issue worldwide. Some countries, including France, have engaged in research into the causes of Parkinson's disease, Alzheimer's disease, and multiple sclerosis and the management of these patients. It should lead to a better understanding of the mechanisms leading to these diseases including the possible involvement of lipids in their pathogenesis. Parkinson's disease is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the accumulation of α-synuclein (Lewy bodies). Several in vivo studies have shown a relationship between the lipid profile [cholesterol, oxidized cholesterol products (oxysterols) formed either enzymatically or by auto-oxidation], the use of drugs regulating cholesterol levels, and the development of Parkinson's disease. Several oxysterols are present in the brain and could play a role in the development of this disease, particularly in the accumulation of α-synuclein, and through various side effects, such as oxidation, inflammation, and cell death. Consequently, in Parkinson's disease, some oxysterols could contribute to the pathophysiology of the disease and constitute potential biomarkers or therapeutic targets.
    Language English
    Publishing date 2016-12
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2016.10.008
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  4. Article: Induction of oxiapoptophagy, a mixed mode of cell death associated with oxidative stress, apoptosis and autophagy, on 7-ketocholesterol-treated 158N murine oligodendrocytes: Impairment by α-tocopherol

    Nury, Thomas / Zarrouk, Amira / Vejux, Anne / Doria, Margaux / Riedinger, Jean Marc / Delage-Mourroux, Régis / Lizard, Gérard

    Biochemical and biophysical research communications. 2014 Apr. 11, v. 446

    2014  

    Abstract: 7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, ...

    Abstract 7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, was to bring new evidence on this mixed form of cell death. On 158N cells, 7KC induces an overproduction of reactive oxygen species (ROS) revealed by dihydroethidium staining, a loss of transmembrane mitochondrial potential measured with DiOC6(3), caspase-3 activation, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC enhances cytoplamic membrane permeability to propidium iodide, and induces acidic vesicular organelle formation evaluated with acridine orange. In addition, 7KC promotes conversion of microtubule-associated protein light chain 3 (LC3-I) to LC3-II which is characteristic of autophagy. These different side effects were impaired by α-tocopherol. Altogether, our data demonstrate that oxiapoptophagy including ROS overproduction, apoptosis and autophagy could be a particular type of cell death activated by 7KC which can be inhibited by α-tocopherol.
    Keywords acridine orange ; adverse effects ; alpha-tocopherol ; apoptosis ; autophagy ; caspase-3 ; membrane permeability ; mice ; mitochondria ; oligodendroglia ; oxidation ; oxidative stress ; propidium ; reactive oxygen species ; staining
    Language English
    Dates of publication 2014-0411
    Size p. 714-719.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2013.11.081
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Induction of oxiapoptophagy, a mixed mode of cell death associated with oxidative stress, apoptosis and autophagy, on 7-ketocholesterol-treated 158N murine oligodendrocytes: impairment by α-tocopherol.

    Nury, Thomas / Zarrouk, Amira / Vejux, Anne / Doria, Margaux / Riedinger, Jean Marc / Delage-Mourroux, Régis / Lizard, Gérard

    Biochemical and biophysical research communications

    2013  Volume 446, Issue 3, Page(s) 714–719

    Abstract: 7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, ...

    Abstract 7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, was to bring new evidence on this mixed form of cell death. On 158N cells, 7KC induces an overproduction of reactive oxygen species (ROS) revealed by dihydroethidium staining, a loss of transmembrane mitochondrial potential measured with DiOC6(3), caspase-3 activation, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC enhances cytoplamic membrane permeability to propidium iodide, and induces acidic vesicular organelle formation evaluated with acridine orange. In addition, 7KC promotes conversion of microtubule-associated protein light chain 3 (LC3-I) to LC3-II which is characteristic of autophagy. These different side effects were impaired by α-tocopherol. Altogether, our data demonstrate that oxiapoptophagy including ROS overproduction, apoptosis and autophagy could be a particular type of cell death activated by 7KC which can be inhibited by α-tocopherol.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Autophagy/drug effects ; Cell Death/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Ketocholesterols/pharmacology ; Mice ; Microscopy, Phase-Contrast/methods ; Microtubule-Associated Proteins/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/drug effects ; Oxidative Stress/drug effects ; alpha-Tocopherol/pharmacology
    Chemical Substances Ketocholesterols ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins ; alpha-Tocopherol (H4N855PNZ1) ; 7-ketocholesterol (O7676FE78M)
    Language English
    Publishing date 2013-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2013.11.081
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Induction of oxiapoptophagy on 158N murine oligodendrocytes treated by 7-ketocholesterol-, 7β-hydroxycholesterol-, or 24(S)-hydroxycholesterol: Protective effects of α-tocopherol and docosahexaenoic acid (DHA; C22:6 n-3).

    Nury, Thomas / Zarrouk, Amira / Mackrill, John J / Samadi, Mohammad / Durand, Philippe / Riedinger, Jean-Marc / Doria, Margaux / Vejux, Anne / Limagne, Emeric / Delmas, Dominique / Prost, Michel / Moreau, Thibault / Hammami, Mohamed / Delage-Mourroux, Régis / O'Brien, Nora M / Lizard, Gérard

    Steroids

    2015  Volume 99, Issue Pt B, Page(s) 194–203

    Abstract: In demyelinating or non-demyelinating neurodegenerative diseases, increased levels of 7-ketocholesterol (7KC), 7β-hydroxycholesterol (7β-OHC) and 24(S)-hydroxycholesterol (24S-OHC) can be observed in brain lesions. In 158N murine oligodendrocytes, 7KC ... ...

    Abstract In demyelinating or non-demyelinating neurodegenerative diseases, increased levels of 7-ketocholesterol (7KC), 7β-hydroxycholesterol (7β-OHC) and 24(S)-hydroxycholesterol (24S-OHC) can be observed in brain lesions. In 158N murine oligodendrocytes, 7KC triggers a complex mode of cell death defined as oxiapoptophagy, involving simultaneous oxidative stress, apoptosis and autophagy. In these cells, 7KC as well as 7β-OHC and 24S-OHC induce a decrease of cell proliferation evaluated by phase contrast microscopy, an alteration of mitochondrial activity quantified with the MTT test, an overproduction of reactive oxygen species revealed by staining with dihydroethidium and dihydrorhodamine 123, caspase-3 activation, PARP degradation, reduced expression of Bcl-2, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC, 7β-OHC and 24S-OHC promote conversion of microtubule-associated protein light chain 3 (LC3-I) to LC3-II which is a characteristic of autophagy. Consequently, 7β-OHC and 24S-OHC, similarly to 7KC, can be considered as potent inducers of oxiapoptophagy. Furthermore, the different cytotoxic effects associated with 7KC, 7β-OHC and 24S-OHC-induced oxiapoptophagy are attenuated by vitamin E (VitE, α-tocopherol) and DHA which enhances VitE protective effects. In 158N murine oligodendrocytes, our data support the concept that oxiapoptophagy, which can be inhibited by VitE and DHA, could be a particular mode of cell death elicited by cytotoxic oxysterols.
    MeSH term(s) Animals ; Anions ; Apoptosis/drug effects ; Autophagy/drug effects ; Biomarkers/metabolism ; Cell Proliferation/drug effects ; Docosahexaenoic Acids/pharmacology ; Hydrogen Peroxide/metabolism ; Hydroxycholesterols/pharmacology ; Ketocholesterols/pharmacology ; Mice ; Microscopy, Phase-Contrast ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oligodendroglia/cytology ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Oxidation-Reduction/drug effects ; Protective Agents/pharmacology ; Superoxides/metabolism ; alpha-Tocopherol/pharmacology
    Chemical Substances Anions ; Biomarkers ; Hydroxycholesterols ; Ketocholesterols ; Protective Agents ; Superoxides (11062-77-4) ; Docosahexaenoic Acids (25167-62-8) ; 24-hydroxycholesterol (47IMW63S3F) ; cholest-5-en-3 beta,7 alpha-diol (566-26-7) ; Hydrogen Peroxide (BBX060AN9V) ; alpha-Tocopherol (H4N855PNZ1) ; 7-ketocholesterol (O7676FE78M)
    Language English
    Publishing date 2015-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80312-1
    ISSN 1878-5867 ; 0039-128X
    ISSN (online) 1878-5867
    ISSN 0039-128X
    DOI 10.1016/j.steroids.2015.02.003
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 87: Show issues Location:
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