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Sci Rep. 2018 Feb 19;8(1):3267. doi: 10.1038/s41598-018-21580-x.

iTRAQ-based quantitative proteomic analysis reveals important metabolic pathways for arsenic-induced liver fibrosis in rats.

Wu S1, Li J2, Jin X2,3.

Author information

1
Department of Occupational and Environmental health, School of public health, Xinjiang Medical University, Urumqi, 830011, China. wsh@xjmu.edu.cn.
2
Department of Occupational and Environmental health, School of public health, Xinjiang Medical University, Urumqi, 830011, China.
3
Shenzhen Omics Medical Research Center, Shenzhen, 518053, China.

Abstract

Long-term consumption of sodium arsenite contaminated water can cause endemic arsenic disease. The proteome profile changes of liver fibrosis after exposure to arsenite containing water remain unclear. In this study, Sprague-Dawley (SD) male rats were treated with sodium arsenite (iAs3+), using a daily dose of 1.36 mg/kg body weight (medium dose group, M), 2.73 mg/kg body weight (high dose group, H) or deionized water (control group, C). Isobaric tags for relative and absolute quantitation (iTRAQ) were used to identify the different abundant proteins (DAPs) after arsenic-induced liver fibrosis. A total of 2987 high-quality proteins were detected (95% confident peptides ≥ 2), 608 of which were differentially expressed (fold change > 2 and p < 0.05) in M group and 475 in H group. Moreover, 431 DAPs were found in both M and H groups and used in subsequent bioinformatic analyses. Gene ontology (GO) analysis revealed 4,709 GO terms could be mapped, among which purine binding, actin filament binding and protein kinase binding were the most enriched terms for molecular function category. In addition, protein-protein interaction analysis showed six clusters of interaction networks. Our data provided new insights into the proteome changes after arsenic-induced liver fibrosis in model rats.

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