1 Howard Hughes Medical Institute, Department of Molecular Biology and the Center for Computational and Integrative Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA
2 Current address: School of Life Sciences, Biotech Building 4-201, Tsinghua University, Beijing 100084, China
Journal of Systems Chemistry 2011, 2:4 doi:10.1186/1759-2208-2-4Published: 1 December 2011
While studying fatty acid vesicles as model primitive cell membranes, we encountered a dramatic phenomenon in which light triggers the sudden rupture of micron-scale dye-containing vesicles, resulting in rapid release of vesicle contents. We show that such vesicle explosions are caused by an increase in internal osmotic pressure mediated by the oxidation of the internal buffer by reactive oxygen species (ROS). The ability to release vesicle contents in a rapid, spatio-temporally controlled manner suggests many potential applications, such as the targeted delivery of cancer chemotherapy drugs, and the controlled deposition of functionalized nanoparticles in microfluidic devices. Recent observations of light-triggered lysosome rupture in vivo suggest the possibility that a common mechanism may underlie light-triggered vesicle explosions and lysosome rupture.