F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome

Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F2-dihomo-isoprostanes (F2-dihomo-IsoPs), peroxidation products from adrenic acid (22...

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Published inJournal of lipid research Vol. 52; no. 12; pp. 2287 - 2297
Main Authors De Felice, Claudio, Signorini, Cinzia, Durand, Thierry, Oger, Camille, Guy, Alexandre, Bultel-Poncé, Valérie, Galano, Jean-Marie, Ciccoli, Lucia, Leoncini, Silvia, D'Esposito, Maurizio, Filosa, Stefania, Pecorelli, Alessandra, Valacchi, Giuseppe, Hayek, Joussef
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2011
American Society for Biochemistry and Molecular Biology
The American Society for Biochemistry and Molecular Biology
Elsevier
Subjects
Online AccessGet full text
ISSN0022-2275
1539-7262
1539-7262
DOI10.1194/jlr.P017798

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Abstract Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F2-dihomo-isoprostanes (F2-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F2-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F2-dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F2-dihomo-IsoP isomers [ent-7(RS)-F2t-dihomo-IsoP and 17-F2t-dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M–181]− precursor ions (m/z 597) produced from both the derivatized ent-7(RS)-F2t-dihomo-IsoP and 17-F2t-dihomo-IsoP. Average plasma F2-dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F2-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT
AbstractList Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F2-dihomo-isoprostanes (F2-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F2-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F2-dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F2-dihomo-IsoP isomers [ent-7(RS)-F2t-dihomo-IsoP and 17-F2t-dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M–181]− precursor ions (m/z 597) produced from both the derivatized ent-7(RS)-F2t-dihomo-IsoP and 17-F2t-dihomo-IsoP. Average plasma F2-dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F2-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT
Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F(2)-dihomo-isoprostanes (F(2)-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F(2)-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F(2)-dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F(2)-dihomo-IsoP isomers [ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M-181](-) precursor ions (m/z 597) produced from both the derivatized ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP. Average plasma F(2)-dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F(2)-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT.Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F(2)-dihomo-isoprostanes (F(2)-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F(2)-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F(2)-dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F(2)-dihomo-IsoP isomers [ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M-181](-) precursor ions (m/z 597) produced from both the derivatized ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP. Average plasma F(2)-dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F(2)-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT.
Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F(2)-dihomo-isoprostanes (F(2)-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F(2)-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F(2)-dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F(2)-dihomo-IsoP isomers [ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M-181](-) precursor ions (m/z 597) produced from both the derivatized ent-7(RS)-F(2t)-dihomo-IsoP and 17-F(2t)-dihomo-IsoP. Average plasma F(2)-dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F(2)-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT.
Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-CpG binding protein 2 gene. Herein, we have synthesized F 2 -dihomo-isoprostanes (F 2 -dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F 2 -dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F 2 -dihomo-IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F 2 -dihomo-IsoP isomers [ent-7(RS)-F 2t -dihomo-IsoP and 17-F 2t -dihomo-IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M–181] − precursor ions ( m/z 597) produced from both the derivatized ent-7(RS)-F 2t -dihomo-IsoP and 17-F 2t -dihomo-IsoP. Average plasma F 2 -dihomo-IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. hese data indicate for the first time that quantification of F 2 -dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT
Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl- CpG binding protein 2 gene. Herein, we have synthesized F2-dihomo-isoprostanes (F2-dihomo-IsoPs), peroxidation products from adrenic acid (22:4 n-6), a known component of myelin, and tested the potential value of F2-dihomo-IsoPs as a novel disease marker and its relationship with clinical presentation and disease progression. F2 - dihomo - IsoPs were determined by gas chromatography/negative-ion chemical ionization tandem mass spectrometry. Newly synthesized F2 - dihomo - IsoP isomers [ent - 7(RS) - F2t - dihomo - IsoP and 17 - F2t - dihomo - IsoP] were used as reference standards. The measured ions were the product ions at m/z 327 derived from the [M-181] precursor ions ( m/z 597) produced from both the derivatized ent - 7(RS) - F2t - dihomo - IsoP and 17 - F2t - dihomo - IsoP. Average plasma F2 - dihomo - IsoP levels in RTT were about one order of magnitude higher than those in healthy controls, being higher in typical RTT as compared with RTT variants, with a remarkable increase of about two orders of magnitude in patients at the earliest stage of the disease followed by a steady decrease during the natural clinical progression. These data indicate for the fi rst time that quantifi cation of F2-dihomo-IsoPs in plasma represents an early marker of the disease and may provide a better understanding of the pathogenic mechanisms behind the neurological regression in patients with RTT
Author Hayek, Joussef
Ciccoli, Lucia
Oger, Camille
Bultel-Poncé, Valérie
Leoncini, Silvia
D'Esposito, Maurizio
De Felice, Claudio
Guy, Alexandre
Galano, Jean-Marie
Filosa, Stefania
Durand, Thierry
Valacchi, Giuseppe
Signorini, Cinzia
Pecorelli, Alessandra
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  surname: De Felice
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  organization: Neonatal Intensive Care Unit, Azienda Ospedaliera Universitaria Senese, Siena, Italy
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  organization: Department of Pathophysiology, Experimental Medicine, and Public Health, University of Siena, Siena, Italy
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  organization: Institut des Biomolécules Max Mousseron, UMR 5247 CNRS – UM I – UM II, Montpellier, France
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  organization: Institut des Biomolécules Max Mousseron, UMR 5247 CNRS – UM I – UM II, Montpellier, France
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  surname: Guy
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  organization: Institut des Biomolécules Max Mousseron, UMR 5247 CNRS – UM I – UM II, Montpellier, France
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  surname: Bultel-Poncé
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– sequence: 8
  givenname: Lucia
  surname: Ciccoli
  fullname: Ciccoli, Lucia
  organization: Department of Pathophysiology, Experimental Medicine, and Public Health, University of Siena, Siena, Italy
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  givenname: Silvia
  surname: Leoncini
  fullname: Leoncini, Silvia
  organization: Department of Pathophysiology, Experimental Medicine, and Public Health, University of Siena, Siena, Italy
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  givenname: Maurizio
  surname: D'Esposito
  fullname: D'Esposito, Maurizio
  organization: Institute of Genetics and Biophysics “Adriano Buzzati Traverso,” CNR, Napoli, Italy
– sequence: 11
  givenname: Stefania
  surname: Filosa
  fullname: Filosa, Stefania
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  fullname: Valacchi, Giuseppe
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  givenname: Joussef
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  fullname: Hayek, Joussef
  organization: Child Neuropsychiatry Unit, University Hospital, Azienda Ospedaliera Universitaria Senese, Siena, Italy
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Copyright 2011 © 2011 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.
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Issue 12
Keywords myelin damage
adrenic acid
autism spectrum disorders
methyl-CpG binding protein 2
Language English
License This is an open access article under the CC BY license.
http://creativecommons.org/licenses/by/4.0
https://www.elsevier.com/tdm/userlicense/1.0
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content type line 23
PMCID: PMC3283260
C. De Felice, C. Signorini, and T. Durand contributed equally to this work.
ORCID 0000-0002-7027-1207
0000-0002-2153-3872
0000-0002-5177-5792
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PublicationTitle Journal of lipid research
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Snippet Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked...
Oxidative damage has been reported in Rett syndrome (RTT), a pervasive developmental disorder caused in up to 95% of cases by mutations in the X-linked methyl-...
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SubjectTerms Adolescent
adrenic acid
Adult
autism spectrum disorders
Biomarkers - blood
Biomarkers - chemistry
Chemical Sciences
Child
Child, Preschool
Disease Progression
Endocrinology and metabolism
Erucic Acids - metabolism
F2-Isoprostanes - blood
F2-Isoprostanes - chemistry
Fatty Acids, Unsaturated
Female
Human health and pathology
Humans
Infant
Life Sciences
Lipid Peroxidation
Medicinal Chemistry
methyl-CpG binding protein 2
myelin damage
Myelin Sheath - metabolism
Organ Specificity
Oxidative Stress
Patient-Oriented and Epidemiological Research
Rett Syndrome - blood
Rett Syndrome - metabolism
Young Adult
Title F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome
URI https://dx.doi.org/10.1194/jlr.P017798
https://www.ncbi.nlm.nih.gov/pubmed/21917727
https://www.proquest.com/docview/904008381
https://hal.science/hal-00744233
https://pubmed.ncbi.nlm.nih.gov/PMC3283260
https://doaj.org/article/4361ec52bf0e41b8aeb2fdf22674420b
Volume 52
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