Author
Listed:
- Adi Tzur-Balter
(Technion—Israel Institute of Technology)
- Zohar Shatsberg
(Institute for Medical Engineering and Science, Massachusetts Institute of Technology)
- Margarita Beckerman
(Institute for Medical Engineering and Science, Massachusetts Institute of Technology)
- Ester Segal
(Technion—Israel Institute of Technology
Russell Berrie Nanotechnology Institute, Technion—Israel Institute of Technology)
- Natalie Artzi
(Institute for Medical Engineering and Science, Massachusetts Institute of Technology
Brigham and Women’s Hospital, Harvard Medical School)
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.
Suggested Citation
Adi Tzur-Balter & Zohar Shatsberg & Margarita Beckerman & Ester Segal & Natalie Artzi, 2015.
"Mechanism of erosion of nanostructured porous silicon drug carriers in neoplastic tissues,"
Nature Communications, Nature, vol. 6(1), pages 1-8, May.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7208
DOI: 10.1038/ncomms7208
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