Regulation of Protein Expression in Mouse Liver by Inorganic Arsenic: Proteomic Analysis

무기비소에 의한 마우스 간의 단백질 발현 조절 : 단백체 분석

  • Jin Bo-Hwan (College of Veterinary Medicine and BK21 Program for Veterinary Science, Seoul National University) ;
  • Seong Je-Kyung (College of Veterinary Medicine and BK21 Program for Veterinary Science, Seoul National University) ;
  • Ryu Doug-Young (College of Veterinary Medicine and BK21 Program for Veterinary Science, Seoul National University)
  • Published : 2006.06.01

Abstract

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), ${\beta}$-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 down-regulated. Summary: Expression of proteins that have been implicated in carcinogenesis, such as HMG-CoA, ${\beta}$-actin, and RACK1, was regulated in the liver of mice transplacentally exposed to inorganic arsenic.

Keywords

References

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