siRNA-mediated AMPKα1 subunit gene PRKAA1 silencing enhances methylmercury toxicity in HEK293 cells

Gi Wook Hwang, Mayumi Tobita, Tsutomu Takahashi, Shusuke Kuge, Kayoko Kita, Akira Naganuma

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The environmental pollutant methylmercury is a potent neurotoxin. The mechanisms of toxicity and biological defense remain largely unknown. We found that inhibiting the expression of PRKAA1 (AMPKα1), an activated subunit of AMP-activated protein kinase (AMPK), increased susceptibility of HEK293 cells to methylmercury toxicity. Treatment of the cells with AICAR (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside), an AMPK activator, reduced the methylmercury toxicity. Here, we suggest for the first time that the activation (phosphorylation) of AMPK may play an important role in reducing the toxicity of methylmercury.

Original languageEnglish
Pages (from-to)601-604
Number of pages4
JournalJournal of Toxicological Sciences
Volume35
Issue number4
DOIs
Publication statusPublished - 2010 Aug 1

Keywords

  • AICAR
  • AMP-activated protein kinase
  • Methylmercury
  • PRKAA1 (AMPKα1)

ASJC Scopus subject areas

  • Toxicology

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