Abstract
A panel of genetically-engineered Escherichia coli biosensor bacteria, responsive to chemical stressors inducing heat shock, DNA damage, oxidative stress (peroxide- and superoxide-type) and fatty acid metabolism interference, was used to characterize the chemical effect of CdSe quantum dot exposure. Results implicate a primary mode of superoxide-type stress toxicity that is dependent upon quantum dot dose, size, and chain length of capping agent, and are consistent with results from other reports employing mammalian cell lines. Imaging studies confirm association of quantum dots with lipophilic regions of the biosensor bacteria (i.e., inner/outer membranes, cell wall, periplasmic space), and demonstrate intracellular alteration of the quantum dot lattice. Corroboratory experiments with superoxide stress mutants and antioxidant amendments confirm oxidative stress while also implicating destabilization of quantum dots.