Toxicol Res.  2013 Dec;29(4):235-240.

Mercury induced the Accumulation of Amyloid Beta (Abeta) in PC12 Cells: The Role of Production and Degradation of Abeta

Affiliations
  • 1Department of Preventive Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. bschoi@cau.ac.kr

Abstract

Extracellular accumulation of amyloid beta protein (Abeta) plays a central role in Alzheimer's disease (AD). Some metals, such as copper, lead, and aluminum can affect the Abeta accumulation in the brain. However, the effect of mercury on Abeta accumulation in the brain is not clear. Thus, this study was proposed to estimate whether mercury concentration affects Abeta accumulation in PC12 cells. We treated 10, 100, and 1000 nM HgCl2 (Hg) or CH3HgCl2 (MeHg) for 48 hr in PC12 cells. After treatment, Abeta40 in culture medium increased in a dose- and time-dependent manner. Hg and MeHg increased amyloid precursor protein (APP), which is related to Abeta production. Neprilysin (NEP) levels in PC12 cells were decreased by Hg and MeHg treatment. These results suggested that Hg induced Abeta accumulation through APP overproduction and reduction of NEP.

Keyword

Alzheimer's disease; Amyloid beta; Mercury; Amyloid precursor protein; beta-Secretase; Neprilysin

MeSH Terms

Aluminum
Alzheimer Disease
Amyloid beta-Peptides
Amyloid Precursor Protein Secretases
Amyloid*
Animals
Brain
Copper
Mercuric Chloride
Metals
Neprilysin
PC12 Cells*
Aluminum
Amyloid
Amyloid Precursor Protein Secretases
Amyloid beta-Peptides
Copper
Mercuric Chloride
Metals
Neprilysin
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