Now, synthesis, optical properties, and surface chemistry of QDs are all well optimized therefore, the preparation of bioconjugated QDs is not a problem anymore. The potential of QDs for cancer imaging was tested for in vitro and in vivo imaging and PDT of cancer. This chapter introduces a variety of methods for interfacing QDs with cells, and the versatility of QDs conjugated with polymers, proteins, peptides, antibodies, ligands, and PS drugs for specific and nonspecific imaging of cells, subcellular organelles, and single molecules as well as PDT. The important property of QDs in bioimaging is its bright and stable fluorescence of choice.
Mitsuru Ishikawa, Vasudevanpillai Biju, in Progress in Molecular Biology and Translational Science, 2011 VI Concluding Remarks The estrogenic effects exerted by QDs were completely suppressed in cells treated with an estrogen receptor antagonist, indicating that the Q D-induced estrogenic signaling is mediated by the estrogen receptor ( Jain et al., 2012).
Green QDs caused more robust estrogenic effect than orange (larger) QDs. (2012) reported that CdTe QDs induce cellular proliferation and estrogen-like effects, comparable to, or even exceeding, those caused by 17β-estradiol. Using the same cell line (MCF-7), Jain et al. In addition, significant global hypoacetylation was observed, implying an epigenomic response ( Choi et al., 2008).
Indeed chromatin reorganization was detected upon exposure of MCF-7 cells to low amounts (5 μg/mL) of green (smaller) CdTe QDs for 24 h. Modifications to chromatin and histones constitute epigenetic changes that may lead to long-term effects on gene expression programming after the exposure has been removed. QDs seem to be capable of accumulating in the nuclei and nucleoli of living human cells, and it has been suggested that QDs preferentially bind to the positively charged core histone proteins, as opposed to DNA or RNA molecules ( Conroy et al., 2008). mitochondria-mediated, apoptosis ( Yan et al., 2011). It was shown that exposure of HUVECs to CdTe QDs for 24 h (10 μg/mL) induced intrinsic, i.e. The toxicity of acid-coated CdTe QDs toward human umbilical vein endothelial cells (HUVECs), which model vascular endothelial cells, was tested at QD concentrations between 0.1 and 100 μg/mL (corresponding to the doses commonly used for in vivo imaging). If QDs are injected intravenously they will circulate in the bloodstream and possibly come into contact with vascular endothelial cells, which may promote atherosclerosis and cardiovascular disease. Interestingly, however, when compared to the intracellular concentrations after exposure to CdCl 2, it was obvious that the toxic effects of CdTe QDs cannot only be attributed to the Cd 2+ ( Winnik and Maysinger, 2013). Indeed, when the intracellular concentrations of Cd 2+ were compared following cellular exposure to the different QDs, it was found that the concentration of CdSe/ZnS was below 5 nM, whereas for CdTe QDs, the concentrations ranged between 30 and 150 nM. The fact that CdSe/ZnS QDs are significantly less toxic than “bare” CdTe QDs suggests that their toxicity is mainly caused by a gradual release of Cd 2+, a well-known toxicant. CdSe/ZnS QDs, show much less toxicity and thus seem more suitable for experiments in living cells exposed for longer periods (hours and even days). Results from studies employing different QD concentrations, different exposure times, and different cell types have thus indicated that (1) cadmium-containing QDs, most prominently CdTeQDs, are the most deleterious to the cells and (2) QDs with multiple shells, e.g. QDs may exert adverse effects on biological systems ( Winnik and Maysinger, 2013). Bengt Fadeel, in Handbook on the Toxicology of Metals (Fourth Edition), 2015 16.2 In Vitro Toxicity Studies
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