Silver impairs neurodevelopment: studies in PC12 cells.

Journal Article (Journal Article)

BACKGROUND: Exposure to silver is increasing because of silver nanoparticles in consumer products. OBJECTIVES AND METHODS: Many biological effects of silver entail actions of Ag+ (monovalent silver ions), so we used neuronotypic PC12 cells to evaluate the potential for silver to act as a developmental neurotoxicant, using chlorpyrifos (CPF), a pesticide known to evoke developmental neurotoxicity, as a positive control for comparison. RESULTS: In undifferentiated cells, a 1-hr exposure to 10 microM Ag+ inhibited DNA synthesis more potently than did 50 microM CPF; it also impaired protein synthesis but to a lesser extent than its effect on DNA synthesis, indicating a preferential effect on cell replication. Longer exposures led to oxidative stress, loss of viability, and reduced numbers of cells. With the onset of cell differentiation, exposure to 10 microM Ag+ evoked even greater inhibition of DNA synthesis and more oxidative stress, selectively impaired neurite formation without suppressing overall cell growth, and preferentially suppressed development into the acetylcholine phenotype in favor of the dopamine phenotype. Lowering the exposure to 1 microM Ag+ reduced the net effect on undifferentiated cells. However, in differentiating cells, the lower concentration produced an entirely different pattern, enhancing cell numbers by suppressing ongoing cell death and impairing differentiation in parallel for both neurotransmitter phenotypes. CONCLUSIONS: Our results show that silver has the potential to evoke developmental neurotoxicity even more potently than known neurotoxicants, such as CPF, and that the spectrum of effects is likely to be substantially different at lower exposures that do not show signs of outright toxicity.

Full Text

Duke Authors

Cited Authors

  • Powers, CM; Wrench, N; Ryde, IT; Smith, AM; Seidler, FJ; Slotkin, TA

Published Date

  • January 2010

Published In

Volume / Issue

  • 118 / 1

Start / End Page

  • 73 - 79

PubMed ID

  • 20056586

Pubmed Central ID

  • PMC2831971

Electronic International Standard Serial Number (EISSN)

  • 1552-9924

Digital Object Identifier (DOI)

  • 10.1289/ehp.0901149


  • eng

Conference Location

  • United States