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Proteomic analysis using isobaric tags for relative and absolute quantification technology reveals mechanisms of toxic effects of tris (1,3-dichloro-2-propyl) phosphate on RAW264.7 macrophage cells

文献类型： 外文期刊

作者： Zhang, Wei 1 ; Wang, Ruiguo 1 ; Giesy, John P. 2 ; Zhang, Su 1 ; Wei, Shulin 1 ; Wang, Peilong 1 ;

作者机构： 1.Chinese Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, 12 Zhongguancun South St, Beijing 100081, Peoples R China

2.Univ Saskatchewan, Dept Vet Biomed Sci, Saskatoon, SK, Canada

3.Univ Saskatchewan, Toxicol Ctr, Saskatoon, SK, Canada

4.Michigan State Univ, Dept Zool, E Lansing, MI 48824 USA

5.Michigan State Univ, Ctr Integrat Toxicol, E Lansing, MI USA

6.Baylor Univ, Dept Environm Sci, Waco, TX 76798 USA

7.Nanjing Univ, Sch Environm, State Key Lab Pollut Control & Resource Reuse, Nanjing, Peoples R China

关键词： apoptosis; iTRAQ; proteomics; RAW264.7 cells; toxicology; tris (1,3-dichloro-2-propyl) phosphate

期刊名称：JOURNAL OF APPLIED TOXICOLOGY （ 影响因子：2.997； 五年影响因子：3.131 ）

ISSN： 0260-437X

年卷期：

页码：

收录情况： SCI

摘要： Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is one of the most commonly used organophosphorus flame retardants. Immuno-toxicity induced by TDCIPP is becoming of increasing concern. However, effects of TDCIPP on immune cells and mechanisms resulting in those effects are poorly understood. In this study, it was determined, for the first time, by use of isobaric tags for relative and absolute quantification (iTRAQ) based proteomic techniques expression of global proteins in RAW264.7 cells exposed to 10 mu M TDCIPP. A total of 180 significantly differentially expressed proteins (DEPs) were identified. Of these, 127 were up-regulated and 53 were down-regulated. The DEPs associated with toxic effects of TDCIPP were then screened by use of Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes for enrichment analysis. Results showed that these DEPs were involved in a number of pathways including apoptosis, DNA damage, cell cycle arrest, immune-toxicity, and signaling pathways, such as the Toll-like receptor, PPAR and p53 signaling pathways. The complex regulatory relationships between different DEPs, which might play an important role in cell death were also observed in the form of a protein-protein interaction network. Meanwhile, mitochondrial membrane potential (MMP) in RAW264.7 cells after TDCIPP treatment was also analyzed, the collapse of the MMP was speculated to play an important role in TDCIPP induced apoptosis. Moreover, some of the important regulator proteins discovered in this study, such as Chk1, Aurora A, would provide novel insight into the molecular mechanisms involved in toxic responses to TDCIPP.

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