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题名: Metabolic Response to Oral Microcystin-LR Exposure in the Rat by NMR-Based Metabonomic Study
作者: He, Jun1; Chen, Jun1; Wu, Laiyan1, 2; Li, Guangyu1, 3; Xie, Ping1
通讯作者: Chen, J (reprint author), Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol China, Donghu Expt Stn Lake Ecosyst, Donghu S Rd 7, Wuhan 430072, Peoples R China.
关键词: microcystin-LR ; metabonomics ; NMR ; glutathione ; choline ; nutrient absorption
刊名: JOURNAL OF PROTEOME RESEARCH
发表日期: 2012-12-01
DOI: 10.1021/pr300685g
卷: 11, 期:12, 页:5934-5946
收录类别: SCI
文章类型: Article
部门归属: [He, Jun; Chen, Jun; Wu, Laiyan; Li, Guangyu; Xie, Ping] Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol China, Donghu Expt Stn Lake Ecosyst, Wuhan 430072, Peoples R China; [Wu, Laiyan] S Cent Univ Nationalities, Coll Chem & Mat Sci, Wuhan 430074, Peoples R China; [Li, Guangyu] Huazhong Agr Univ, Coll Fisheries, Wuhan, Peoples R China
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
资助者: National Natural Science Foundation of China [31070457]
类目[WOS]: Biochemical Research Methods
研究领域[WOS]: Biochemistry & Molecular Biology
摘要: Microcystin-LR (MCLR), a potent hepatotoxin, is causing increased risks to public health. Although the liver is the main target organ of MCLR, the metabolic profiling of liver in response to MCLR in vivo remains unknown. Here, we comprehensively analyzed the metabolic change of liver and ileal flushes in rat orally gavaged with MCLR by H-1 nuclear magnetic resonance (NMR). Quantification of hepatic MCLR and its glutathione and cysteine conjugates by liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) was conducted. Metabonomics results revealed significant associations of MCLR-induced disruption of hepatic metabolisms with inhibition of nutrient absorption, as evidenced by a severe decrease of 12 amino acids in the liver and their corresponding elevation in ileal flushes. The hepatic metabolism signature of MCLR was characterized by significant inhibition of tyrosine anabolism and catabolism, three disrupted pathways of choline metabolism, glutathione exhaustion, and disturbed nucleotide synthesis. Notably, substantial alterations of hepatic metabolism were observable even at the low MCLR-treated group (0.04 mg/kg MCLR), although no apparent histological changes in liver were observed in the low- and medium-dosed groups. These observations offered novel insights into the microcystin hepatotoxic mechanism at a functional level, thereby facilitating further assessment and clarification of human health risk from MCs exposure.
英文摘要: Microcystin-LR (MCLR), a potent hepatotoxin, is causing increased risks to public health. Although the liver is the main target organ of MCLR, the metabolic profiling of liver in response to MCLR in vivo remains unknown. Here, we comprehensively analyzed the metabolic change of liver and ileal flushes in rat orally gavaged with MCLR by H-1 nuclear magnetic resonance (NMR). Quantification of hepatic MCLR and its glutathione and cysteine conjugates by liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) was conducted. Metabonomics results revealed significant associations of MCLR-induced disruption of hepatic metabolisms with inhibition of nutrient absorption, as evidenced by a severe decrease of 12 amino acids in the liver and their corresponding elevation in ileal flushes. The hepatic metabolism signature of MCLR was characterized by significant inhibition of tyrosine anabolism and catabolism, three disrupted pathways of choline metabolism, glutathione exhaustion, and disturbed nucleotide synthesis. Notably, substantial alterations of hepatic metabolism were observable even at the low MCLR-treated group (0.04 mg/kg MCLR), although no apparent histological changes in liver were observed in the low- and medium-dosed groups. These observations offered novel insights into the microcystin hepatotoxic mechanism at a functional level, thereby facilitating further assessment and clarification of human health risk from MCs exposure.
关键词[WOS]: TYPE-2A PROTEIN PHOSPHATASES ; GENE-EXPRESSION CHANGES ; HEPATOTOXIC MICROCYSTINS ; CARDIOVASCULAR-DISEASE ; GLUTATHIONE CONJUGATE ; QUANTITATIVE-ANALYSIS ; MOLECULAR-MECHANISMS ; INHIBITORY-ACTIVITY ; DNA METHYLATION ; BIGHEAD CARP
语种: 英语
WOS记录号: WOS:000311925900033
ISSN号: 1535-3893
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/19301
Appears in Collections:淡水生态学研究中心_期刊论文

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作者单位: 1.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol China, Donghu Expt Stn Lake Ecosyst, Wuhan 430072, Peoples R China
2.S Cent Univ Nationalities, Coll Chem & Mat Sci, Wuhan 430074, Peoples R China
3.Huazhong Agr Univ, Coll Fisheries, Wuhan, Peoples R China
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