ABSTRACT
Oxidative toxicity of semiconductor and metal nanomaterials to cells has been well established. However, it may result from many different mechanisms, some requiring direct cell contact and others resulting from the diffusion of reactive species in solution. Published results are contradictory due to differences in particle preparation, bacterial strain, and experimental conditions. It has been recently found that C(60) nanoparticles can cause direct oxidative damage to bacterial proteins and membranes, including causing a loss of cell membrane potential (depolarization). However, this did not correlate with toxicity. In this study we perform a similar analysis using fluorescent CdTe quantum dots, adapting our tools to make use of the particles' fluorescence. We find that two Gram positive strains show direct electron transfer to CdTe, resulting in changes in CdTe fluorescence lifetimes. These two strains also show changes in membrane potential upon nanoparticle binding. Two Gram negative strains do not show these effects-nevertheless, they are over 10-fold more sensitive to CdTe than the Gram positives. We find subtoxic levels of Cd(2+) release from the particles upon irradiation of the particles, but significant production of hydroxyl radicals, suggesting that the latter is a major source of toxicity. These results help establish mechanisms of toxicity and also provide caveats for use of certain reporter dyes with fluorescent nanoparticles which will be of use to anyone performing these assays. The findings also suggest future avenues of inquiry into electron transfer processes between nanomaterials and bacteria.
Subject(s)
Cadmium/toxicity , Gram-Negative Bacteria/drug effects , Gram-Negative Bacteria/metabolism , Gram-Positive Bacteria/drug effects , Gram-Positive Bacteria/metabolism , Nanoparticles/toxicity , Quantum Dots , Tellurium/toxicity , Nanotechnology , Semiconductors/adverse effectsABSTRACT
The response of water-soluble, mercaptocarboxylic acid-capped fluorescent semiconductor nanoparticles, or quantum dots (QDs), to extended visible-light irradiation is variable and poorly described. Here we use time-resolved spectroscopy to investigate the photoluminescence intensities and lifetimes of CdSe/ZnS and CdTe QDs as a function of blue light illumination. Conjugates of the particles to the electron donor dopamine were also investigated, and the effect of the antioxidant beta-mercaptoethanol was explored. Both types of QD showed signs of direct electron transfer to the conjugate, but enhancement was much more pronounced in CdSe/ZnS. A model of the two different types of enhancement is proposed.
Subject(s)
Cadmium Compounds/chemistry , Dopamine/chemistry , Quantum Dots , Selenium Compounds/chemistry , Sulfides/chemistry , Tellurium/chemistry , Zinc Compounds/chemistry , Luminescence , Oxygen/chemistry , Photons , Time FactorsABSTRACT
Semiconductor quantum dots (QDs) have been widely used for fluorescent labelling. However, their ability to transfer electrons and holes to biomolecules leads to spectral changes and effects on living systems that have yet to be exploited. Here we report the first cell-based biosensor based on electron transfer between a small molecule (the neurotransmitter dopamine) and CdSe/ZnS QDs. QD-dopamine conjugates label living cells in a redox-sensitive pattern: under reducing conditions, fluorescence is only seen in the cell periphery and lysosomes. As the cell becomes more oxidizing, QD labelling appears in the perinuclear region, including in or on mitochondria. With the most-oxidizing cellular conditions, QD labelling throughout the cell is seen. Phototoxicity results from the creation of singlet oxygen, and can be reduced with antioxidants. This work suggests methods for the creation of phototoxic drugs and for redox-specific fluorescent labelling that are generalizable to any QD conjugated to an electron donor.
