KMID : 0382320060260020035
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Environmental Mutagens and Carcinogens 2006 Volume.26 No. 2 p.35 ~ p.40
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Regulation of Protein Expression in Mouse Liver by Inorganic Arsenic: Proteomic Analysis
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Jin Bo-Hwan
Seong Je-Kyung Ryu Doug-Young
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Abstract
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Background: Inorganic arsenic is a human carcinogen that can target the liver, but its carcinogenic mechanisms are still unknown. Inorganic arsenic induces a spectrum of tumors including hepatocellular carcinoma in mice. Methods: Pregnant C3H mice were supplied with drinking water containing 50 ppm sodium arsenite during their pregnancy. The protein expression profile in the liver of 0.5-day-old male offsprings exposed transplacentally to sodium arsenite was analyzed using protein 2D gel electrophoresis followed by mass spectrometry (MALDI-TOF). Results: Expression of proteins such as hydroxymethylglutaryl-CoA synthase mitochondrial precursor (HMG-CoA synthase), ¥â-actin (cytoplasmic 1) and apolipoprotein A-IV precursor (Apo-AIV) were induced in mouse liver by sodium arsenite, while uricase (urate oxidase), guanine nucleotidebinding protein beta subunit 2-like 1 (RACK1) and fructose-bisphosphate aldolase B (Aldolase 2) were downregulated. Summary: Expression of proteins that have been implicated in carcinogenesis, such as HMG-CoA, ¥â-actin, and RACK1, was regulated in the liver of mice transplacentally exposed to inorganic arsenic.
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KEYWORD
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arsenic, water, liver, mouse, HMG-CoA synthase, RACK1, proteomics
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