Abstract
Here we report the synthesis and in vitro characterization of a redox-sensitive, magnetically inducible nanoparticle carrier system based on the doxorubicin (DOX) drug delivery model. Each quantal nanocarrier unit consists of a magnetite Fe3O4 nanoparticle core that is further encapsulated in self-assembled micelles of the redox-responsive polyethylene glycol derivative, DSPE-SS-mPEG. The nanocarrier system was prepared using a combination of ultrasonication and dialysis to produce the microenvironment sensitive delivery system. The final synthesized and DOX-loaded magnetic nanocarriers had an average size of ~150 nm when assembled with a 6.9% DOX payload. The release rate of DOX from these redox-responsive magnetic nanocarriers was shown to be accelerated in vitro when in the presence of glutathione (GSH). Furthermore, we demonstrated that more redox-responsive magnetic nanocarriers could be taken up by HeLa cells when a local magnetic field was applied. Once internalized within a cell, the micelles of the outer nanocarrier complex were broken down in the presence of higher concentrations of GSH, which accelerated the release of DOX. This produces a particle with dual operating characteristics that can be controlled via a specific cellular environment coupled with an exogenously applied signal in the form of a magnetic field triggering release.
Highlights
Chemotherapy is the most commonly used approach to treating cancer
Because DSPE-SS-mPEG does not significantly attenuate electron scattering under transmission electron microscopy (TEM), nanocarriers are largely present as isolated clusters of Fe3O4 nanoparticles with a spherical shape
We use the amphiphilic copolymer DSPE-SSmPEG, which is connected by disulfide bonds
Summary
The chemotherapeutic agents (doxorubicin, paclitaxel, etc.) are systemically delivered through intravenous injection While this is often an effective approach and can successfully eliminate malignant cell populations, treatment-associated morbidity is often significant [1]. Quite frequently this is a result of unintended action of the therapeutic agent at non-specific cellular targets causing injury to healthy somatic cells in addition to the desired effect on malignant cells [2,3,4,5,6]. At the intersection of the potency of chemotherapy as a curative agent and the extensive side effect
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