A proteomic method for analysis of CYP450s protein expression changes in carbon tetrachloride induced male rat liver microsomes

Jia, Ning; Liu, Xin; Wen, Jing; Qian, Linyi; Qian, Xiaohong; Wu, Yutian; Fan, Guorong

doi:10.1016/j.tox.2007.04.015

Cited by 34 publications

(18 citation statements)

References 30 publications

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“…Jia et al (2007) found that the hepatoxicity induced in vivo by CCl 4 administration altered the expression of 17 cytochrome P450 proteins. The results of microarray analysis agree with previous studies by showing that hepatic fibrosis induced by CCl 4 is associated with significant changes in the expression of genes related to oxidative stress and cytochrome P450.…”

Section: Discussionmentioning

confidence: 97%

Hepatoprotective effects and mechanisms of dehydrocavidine in rats with carbon tetrachloride-induced hepatic fibrosis

Wang

Zhao

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 97%

Hepatoprotective effects and mechanisms of dehydrocavidine in rats with carbon tetrachloride-induced hepatic fibrosis

Wang

Zhao

et al. 2011

Journal of Ethnopharmacology

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“…Cytochrome P-450 (CYP) is known to be involved in metabolism of drugs, chemicals, and endogenous substrates. In addition, hepatic CYPs are involved in pathogenesis of several liver diseases (36,37). Among them, elevated CYP2E1 has been reported to enhance cisplatin-induced hepatotoxicity, and increased ROS and oxidative stress are suggested as the toxic mechanisms in vivo (11,38) and in vitro (11).…”

Section: Expression Of Proteins and Genes Associated With Drug Metabomentioning

confidence: 99%

In-depth Identification of Pathways Related to Cisplatin-induced Hepatotoxicity through an Integrative Method Based on an Informatics-assisted Label-free Protein Quantitation and Microarray Gene Expression Approach

Cho

Singh

Lee

et al. 2012

Molecular & Cellular Proteomics

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Cisplatin is used widely for treatment of a variety of cancer diseases. Recently, however, the use of cisplatin is restricted because of its adverse effects such as hepatotoxicity. There is no study with current proteomics technology to evaluate cisplatin-induced hepatotoxicity, even if some studies have reported on the hepatotoxicity. In this study, proteomic as well as genomic analyses have been used for identification of proteins and genes that respond to cisplatin treatment in rat primary hepatocytes. To investigate the hepatotoxic effects of cisplatin, rat primary hepatocytes were treated with an IC 20 concentration for 24 h. From proteomic analysis based on label-free quantitation strategy, cisplatin induced 76 up-regulated and 19 down-regulated proteins among 325 distinct proteins. In the mRNA level, genomic analysis revealed 72 up-regulated and 385 down-regulated genes in the cisplatin-treated group. Based on these two analyses, 19 pathways were commonly altered, whereas seven pathways were identified only by proteomic analysis, and 19 pathways were identified only by genomic analysis. Overall, this study explained the mechanism of cisplatin-induced hepatotoxicity with two points of view: well known pathways including drug metabolism, fatty acid metabolism, and glycolysis/TCA cycle and little known pathways including urea cycle and inflammation metabolism, for hepatotoxicity of other toxic agents. Up-regulated proteins detected by proteomic analysis in the cisplatin-treated group: FBP1 (fructose 1,6-bisphosphatase 1), FASN (fatty acid synthase), CAT (catalase), PRDX1 (peroxiredoxin-1), HSPD1 (60-kDa heat shock protein), MDH2 (malate dehydrogenase 2), and ARG1 (arginase 1), and also downregulated proteins in the cisplatin-treated group: TPM1 (tropomyosin 1), TPM3 (tropomyosin 3), and CTSB (cathepsin B), were confirmed by Western blot analysis. In addition, up-regulated mRNAs detected by microarray analysis in the cisplatin-treated group: GSTA2, GSTT2, YC2, TXNRD1, CYP2E1, CYP2C13, CYP2D1, ALDH17, ARG1, ARG2, and IL-6, and also down-regulated mRNAs: CYP2C12, CYP26B1, TPM1, and TPM3, were confirmed by RT-PCR analysis. In case of PRDX1, FASN, and ARG1, they were further confirmed by immunofluorescence analysis. Through the integrated proteomic and genomic approaches, the present study provides the first pathway map related to cisplatin-induced hepatotoxicity, which may provide new insight into the mechanism of hepatotoxicity. Molecular & Cellular

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“…This approach not only reveals the identity of a protein 76 but also provides unparalleled sensitivity and selectivity for pro-77 tein quantitation [10,11]. Although isotope labeling techniques 78 are widely used for quantification of CYP450 enzymes [12][13][14] Peak area ratios (y) are ratio of peak area of metabolism enzymes peptides to that of yeast enolase peptide (IS) and x is for concentration of metabolism enzymes (n = 3). a Expressed as coefficient of variation (standard deviation/mean) Â 100. b Expressed as extraction recovery: determined by comparing the peak areas of the peptides obtained from samples spiked into rat liver microsomes and postextraction.…”

mentioning

confidence: 99%

Targeted label-free approach for quantification of epoxide hydrolase and glutathione transferases in microsomes

Song

Peng

2015

Analytical Biochemistry

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A proteomic method for analysis of CYP450s protein expression changes in carbon tetrachloride induced male rat liver microsomes

Cited by 34 publications

References 30 publications

Hepatoprotective effects and mechanisms of dehydrocavidine in rats with carbon tetrachloride-induced hepatic fibrosis

Hepatoprotective effects and mechanisms of dehydrocavidine in rats with carbon tetrachloride-induced hepatic fibrosis

In-depth Identification of Pathways Related to Cisplatin-induced Hepatotoxicity through an Integrative Method Based on an Informatics-assisted Label-free Protein Quantitation and Microarray Gene Expression Approach

Targeted label-free approach for quantification of epoxide hydrolase and glutathione transferases in microsomes

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