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

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.