Stimulation of Cysteine-Coated CdSe/ZnS Quantum Dot Luminescence by meso-Tetrakis (p-sulfonato-phenyl) Porphyrin.

Interaction between porphyrins and quantum dots (QD) via energy and/or charge transfer is usually accompanied by reduction of the QD luminescence intensity and lifetime. However, for CdSe/ZnS-Cys QD water solutions, kept at 276 K during 3 months (aged QD), the significant increase in the luminescence intensity at the addition of meso-tetrakis (p-sulfonato-phenyl) porphyrin (TPPS4) has been observed in this study. Aggregation of QD during the storage provokes reduction in the quantum yield and lifetime of their luminescence. Using steady-state and time-resolved fluorescence techniques, we demonstrated that TPPS4 stimulated disaggregation of aged CdSe/ZnS-Cys QD in aqueous solutions, increasing the quantum yield of their luminescence, which finally reached that of the fresh-prepared QD. Disaggregation takes place due to increase in electrostatic repulsion between QD at their binding with negatively charged porphyrin molecules. Binding of just four porphyrin molecules per single QD was sufficient for total QD disaggregation. The analysis of QD luminescence decay curves demonstrated that disaggregation stronger affected the luminescence related with the electron-hole annihilation in the QD shell. The obtained results demonstrate the way to repair aged QD by adding of some molecules or ions to the solutions, stimulating QD disaggregation and restoring their luminescence characteristics, which could be important for QD biomedical applications, such as bioimaging and fluorescence diagnostics. On the other hand, the disaggregation is important for QD applications in biology and medicine since it reduces the size of the particles facilitating their internalization into living cells across the cell membrane.

Light induced cytotoxicity of nitrofurantoin toward murine melanoma.

The cytotoxicity of nitrofurantoin (NFT) in the dark and after light exposure (UVA irradiation, λ = 385 nm) was evaluated in murine melanoma B16F10 cells. NFT induces both cell proliferation and inhibition of cell viability. The dominance of one or the other effect depends on the drug concentration, incubation time (tinc) and irradiation dose. The uptake of NFT in these cells, as well as its photocytotoxicity, reaches saturation after 24 hours of incubation. The mechanism of cell death in the dark is associated with the enzymatic release of nitric oxide (NO). The increase of NFT cytotoxicity under light irradiation is associated with the increase of NO concentration due to photorelease. NO photorelease by NFT in solution was confirmed by chemiluminescence, while NO formation in cells was confirmed by fluorescence microscopy using DAF-2DA, a specific indicator of NO in living cells. The NFT does not enter nuclei, distributing preferentially in the cell cytoplasm, as shown by fluorescence microscopy.