Using oxidant susceptibility of thiol stabilized nanoparticles to develop an inflammation triggered drug release system.

Inflammation is a complex and dynamic defensive cellular approach to safeguard against deleterious agents; however, an overexpression of such responses frequently results in the development of a number of devastating diseases, such as atherosclerosis, cancer, inflammatory bowel, Alzheimer's and Parkinson's diseases. At the site of the inflammation, excessive amount of reactive oxygen species (ROS) are produced, and therefore researchers are now earnestly trying to exploit ROS pathological signals to design oxidative triggered drug release systems. In this study, we report a straightforward strategy to develop an oxidative stress responsive drug release systems. Newly developed, ultra-small, and thiol stabilized zinc sulfide quantum dots (ZnS QDs) are used as nanocaps to regulate the release of anticancer drug (camptothecin) from mesoporous silica nanoparticles (MSNs) in response to oxidative environment. The exposure of capped nanocarrier to a higher concentration of H₂O₂ fails to open the drug loaded nanochannels; however, an addition of a minute amount of divalent iron, the most abundant transition-metal in the body, readily unseals the nanochannels at considerably lower H₂O₂ concentrations due to the generation of highly reactive hydroxyl radicals (˙OH). Thiol groups, which stabilize the ZnS nanolids, are actually oxidized by ˙OH and as a result unleash the loaded drug molecules from the channels of silica. In addition to the inflammation-induced drug delivery, this study also provides basic insight into the fate of thiol stabilized nanoparticles upon interaction with hydroxyl radicals.