Dynamic energy budget approach to modeling mechanisms of CdSe quantum dot toxicity.

A mechanistic model of bacterial growth based on dynamic energy budget (DEB) theory is utilized to investigate mechanisms of toxicity of CdSe quantum dots (QDs). The model of QD toxicity is developed by extending a previously published DEB model of cadmium ion toxicity to include a separate model of QD toxic action. The extension allows for testing whether toxicity from QD exposure can be explained fully by dissolved cadmium exposure only, or if the separate effects of QDs need to be taken into account as well. Two major classes of QD toxicity mechanisms are considered: acclimation expressed through initial retardation of growth, and three separate metabolic effects that can be a result of QDs either reversibly or irreversibly associating with the cell. The model is consistent with the data, and is able to distinguish toxic effects due to QD nano-particles from the effects due to cadmium ions. Results suggest that, in contrast to ionic exposure where required acclimation remains constant as exposure increases, increase of the energy required for acclimation with exposure is the primary toxic effect of QDs. Reactive oxygen species measurements help conclude that increase in energetic cost of maintenance processes such as cellular repair and maintenance of cross-membrane gradients is the most important of the three metabolic effects of QD toxicity.