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

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?

SUBMITTER: Wu S

PROVIDER: S-EPMC5818499 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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

Wu Shunhua S Li Jing J Jin Xiang X

Scientific reports 20180219 1

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 (iTRA ...[more]

PMID: 29459688

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Project description:Heat stress (HS) is one of the main environmental factors affecting the efficiency of poultry production. The yellow-feather chickens (YFC) as an indigenous strain of chicken is a popular poultry breed in China. Our previous study used the RNA-seq to analyze the gene expression profiles of male YFC under HS and showed that the lipid and energy metabolism pathways are activated in livers of YFC exposed to acute HS (38°C, 4 h and 25°C recovery 2 h). In this study, we used quantitative proteome analysis based on iTRAQ to study the liver response of YFC to cycle chronic HS (38 ± 1°C, 8 h/d, 7 d, CyCHS). The male YFCs treatment used the CyCHS from 22 to 28 days of age. The liver tissue samples were collected at 28 d old. A total of 39,327 unique peptides matches were detected using iTRAQ analysis and 4,571 proteins exhibited a false discovery rate of 1% or less. Forty-six significant differentially expressed proteins (DEPs) were detected in the CyCHS group compared with the control group for the liver samples, including up- and down-regulated DEPs were 18 and 28, respectively. We found that the enriched biological process terms of the DEPs expressed in the liver were related to DNA metabolic process, oxidation-reduction process, oxidative stress and gluconeogenesis. In KEGG pathway analysis. Most of the hepatic DEPs were annotated to glutathione metabolism and TCA cycle in response to CyCHS. The up-regulation of 5 DEPs (GPX1, GSTT1, GSTT1L, RRM2, and LOC100859645) in the glutathione metabolism pathway likely reflects an attempt to deal with oxidative damage by CyCHS. The down-regulation of 3 DEPs (Isocitrate dehydrogenase [IDH3A], IDH3B, and phosphoenolpyruvate carboxykinase 1) in the TCA cycle pathway contributes to the regulation mechanism of energy metabolism and probably to cope with the balance of heat production and dissipation during CyCHS in order to adapt to high temperature environments. Our results provide insights into the potential molecular mechanism in heat-induced oxidative stress and energy in YFCs and future studies will investigate the functional genes associated with the response to HS.

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

Publications

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

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