Document Type

Article

Publication Date

11-2014

Publication Source

Colloids and Surfaces B: Biointerfaces

Abstract

Due to their distinctive physiochemical properties, including a robust antibacterial activity and plasmonic capability, hundreds of consumer and medical products contain colloidal silver nanoparticles (AgNPs). However, even at sub-toxic dosages, AgNPs are able to disrupt cell functionality, through a yet unknown mechanism. Moreover, internalized AgNPs have the potential to prolong this disruption, even after the removal of excess particles. In the present study, we evaluated the impact, mechanism of action, and continual effects of 50 nm AgNP exposure on epidermal growth factor (EGF) signal transduction within a human keratinocyte (HaCaT) cell line. After AgNP expose, EGF signaling was initially obstructed due to the dissolution of particles into silver ions. However, at longer durations, the internalized AgNPs increased EGF signaling activity. This latter behavior correlated to sustained HaCaT stress, believed to be maintained through the continual dissolution of internalized AgNPs. This study raises concerns that even after exposure ceases, the retained nanomaterials are capable of acting as a slow-release mechanism for metallic ions; continually stressing and modifying normal cellular functionality.

Inclusive pages

136–142

ISBN/ISSN

0927-7765

Document Version

Postprint

Comments

The document available for download is the authors' accepted manuscript, provided in compliance with the publisher's policy on self-archiving. Some differences may be present between the document and the version of record.

Permission documentation is on file.

Publisher

Elsevier

Volume

123

Issue

1

Peer Reviewed

yes