Title Lipidomic analysis of p-chlorophenylalanine-treated mice using continuous-flow two-dimensional liquid chromatography/quadrupole time-of-flight mass spectrometry
Authors Weng, Rui
Shen, Sensen
Yang, Li
Li, Min
Tian, Yonglu
Bai, Yu
Liu, Huwei
Affiliation Peking Univ, Beijing Natl Lab Mol Sci, Key Lab Bioorgan Chem & Mol Engn,Minist Educ, Inst Analyt Chem,Coll Chem & Mol Engn, Beijing 100871, Peoples R China.
Peking Univ, Lab Anim Ctr, Beijing 100871, Peoples R China.
Peking Univ, Coll Chem & Mol Engn, Inst Analyt Chem, Beijing 100871, Peoples R China.
Keywords LC-QTOF-MS
ALZHEIMERS-DISEASE
BRAIN-SEROTONIN
PARKINSONS-DISEASE
HUMAN PLASMA
DEPRESSION
METABOLISM
SCHIZOPHRENIA
TRYPTOPHAN
DISORDERS
Issue Date 2015
Publisher RAPID COMMUNICATIONS IN MASS SPECTROMETRY
Citation RAPID COMMUNICATIONS IN MASS SPECTROMETRY.2015,29,(16),1491-1500.
Abstract RATIONALE: Although serotonin deficiency is involved with various physiological disorders such as Alzheimer's disease, Parkinson's disease, schizophrenia and depression, the serotonin-dependent pathomechanisms remain poorly understood, particularly from a lipidomics perspective. METHODS: This study therefore aimed to identify novel lipid biomarkers associated with serotonin deficiency by lipid profiling of p-chlorophenylalanine (pCPA)-treated, serotonin-deficient mice using continuous-flow normal-phase/reversed-phase two-dimensional liquid chromatography/quadrupole time-of-flight mass spectrometry (NP/RP 2D LC/QTOFMS). Principal component analysis (PCA) was performed to distinguish significantly altered lipids between the pCPA-treated mice and control mice. RESULTS: Eighteen lipid biomarkers were associated with pCPA-induced serotonin deficiency. Specifically, lipid species of lysophosphatidylethanolamine (LPE), phosphatidylethanolamine (PE), sphingomyelin (SM), galactosylceramide (GalCer), glucotosylceramide (GluCer), lactosylceramide (LacCer) and triacylglycerol (TG) were down-regulated whereas glycerophosphocholine (PC) and phosphatidylinositol (PI) were up-regulated in the pCPA-treated mice compared with control mice. CONCLUSIONS: This work demonstrates the significant effects of serotonin deficiency on lipid metabolisms and will facilitate improved understanding of pathomechanisms in serotonin deficiency, particularly from a lipidomics perspective. Copyright (C) 2015 John Wiley & Sons, Ltd.
URI http://hdl.handle.net/20.500.11897/417006
ISSN 0951-4198
DOI 10.1002/rcm.7241
Indexed SCI(E)
PubMed
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