Mechanism of erosion of nanostructured porous silicon drug carriers in neoplastic tissues
Name
Tzur-Balter-2015-Mechanism of Erosion.pdf
Size
1.07 MB
Format
Adobe PDF
Checksum (MD5)
1d582bd836e3a5b8c5ec0191e681c7fb
Author(s)
Tzur-Balter, Adi
Shatsberg, Zohar
Beckerman, Margarita
Segal, Ester
Artzi, Natalie
Date Issued
February 2015
Journal
Nature Communications
Publisher
Nature Publishing Group
Citation
Tzur-Balter, Adi, Zohar Shatsberg, Margarita Beckerman, Ester Segal, and Natalie Artzi. “Mechanism of Erosion of Nanostructured Porous Silicon Drug Carriers in Neoplastic Tissues.” Nature Communications 6 (February 11, 2015): 6208.
Version
Final published version
Abstract
Nanostructured porous silicon (PSi) is emerging as a promising platform for drug delivery owing to its biocompatibility, degradability and high surface area available for drug loading. The ability to control PSi structure, size and porosity enables programming its in vivo retention, providing tight control over embedded drug release kinetics. In this work, the relationship between the in vitro and in vivo degradation of PSi under (pre)clinically relevant conditions, using breast cancer mouse model, is defined. We show that PSi undergoes enhanced degradation in diseased environment compared with healthy state, owing to the upregulation of reactive oxygen species (ROS) in the tumour vicinity that oxidize the silicon scaffold and catalyse its degradation. We further show that PSi degradation in vitro and in vivo correlates in healthy and diseased states when ROS-free or ROS-containing media are used, respectively. Our work demonstrates that understanding the governing mechanisms associated with specific tissue microenvironment permits predictive material performance.
MIT Department
Massachusetts Institute of Technology. Institute for Medical Engineering & Science
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1038/ncomms7208
