Quantum dots (QDs), including CdSe/ZnS, are nanoparticles emitting various wavelengths of fluorescent light depending on their size. Fluorescence allows them to be exploited for in vivo sensing/imaging of cancer cells. Nevertheless, thorough assessments of the effects of these commonly used QDs on cell stability are essentially required prior to their full applications. To investigate the effects of Cd QDs on the growth of human cervical cancer cells (HeLa), we utilized a growth assay, a reactive oxygen species (ROS) assay, an apoptosis assay, and RNA-seq. The growth assay results showed significant proliferation inhibition of HeLa cells by CdSe/ZnS. We revealed that smaller green CdSe/ZnS exerts more toxic effects than slightly larger yellow CdSe/ZnS. There were no significant increases of ROSs under the treatment of Cd QDs, which is consistent with the notion that low concentration of Cd QDs does not cause significant production of ROSs. In addition, we found that Cd QDs induced late apoptosis. RNA-Seq-based transcriptome analysis revealed that the exposure to green Cd QDs significantly upregulated antiapoptotic, antiproliferative, and antitumorigenic functions. The transcriptome profile also noted the downregulation of pro-proliferation, mitochondrial respiratory chain, detoxification, and receptor-mediated endocytosis. Taken together, our findings provide evidence that green CdSe/ZnS can be an alternative anticancer drug. In addition, our transcriptome analysis provides new insights into alteration of physiological state induced by CdSe/ZnS QDs in HeLa cancer cells.

The study of the interaction of engineered nanoparticles, including quantum dots (QDs), with cellular constituents and the kinetics of their localization and transport, has provided new insights into their biological consequences in cancers and for the development of effective cancer therapies. The present study aims to elucidate the toxicity and intracellular transport kinetics of CdSe/ZnS and InP/ZnS QDs in late-stage ML-1 thyroid cancer using well-tested HeLa as a control. Our XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) viability assay (Cell Proliferation Kit II) showed that ML-1 cells and non-cancerous mouse fibroblast cells exhibit no viability defect in response to these QDs, whereas HeLa cell viability decreases. These results suggest that HeLa cells are more sensitive to the QDs compared to ML-1 cells. To test the possibility that transporting rates of QDs are different between HeLa and ML-1 cells, we performed a QD subcellular localization assay by determining Pearson’s Coefficient values and found that HeLa cells showed faster QDs transporting towards the lysosome. Consistently, the ICP-OES test showed the uptake of CdSe/ZnS QDs in HeLa cells was significantly higher than in ML-1 cells. Together, we conclude that high levels of toxicity in HeLa are positively correlated with the traffic rate of QDs in the treated cells.

A modified Nafion dispersion for direct screen printing was developed and characterized. Commercial Nafion solution was neutralized to its sodium form and the solvent was replaced by a screen-printing-compatible solvent. The modified Nafion dispersion has optimized rheological properties including shear-thinning behavior, thixotropy, and moderate yield stress. The elemental composition and chemical states of the modified Nafion were characterized by X-ray photoelectron spectroscopy (XPS). The chemical state and composition of the modified Nafion remained the same as those of commercial Nafion. The crystallinity of the cured membranes of both Nafion dispersions was evaluated by X-ray diffraction spectroscopy (XRD). It was found that the modified Nafion has lower crystallinity as compared to the commercial Nafion, and the degree of crystallinity increases with an increase in the curing temperature. The modified material was screen printed onto a commercial sensor as a cation-exchange membrane for the detection of lead Pb(II) in buffer solutions. The sensor showed good linearity in the range of 5 µg/L to 500 µg/L, with a detection limit of 2 µg/L for Pb(II) by square-wave anodic stripping voltammetry. This work demonstrates the possibility of printing Nafion on a large scale in a wide range of fields, such as printed electrochemical sensors.

InP/ZnS quantum dots (QDs) are an emerging option in QD technologies for uses of fluorescent imaging as well as targeted drug and anticancer therapies based on their customizable properties. In this study we explored effects of InP/ZnS when treated with HeLa cervical cancer cells. We employed XTT viability assays, reactive oxygen species (ROS) analysis, and apoptosis analysis to better understand cytotoxicity extents at different concentrations of InP/ZnS. In addition, we compared the transcriptome profile from the QD-treated HeLa cells with that of untreated HeLa cells to identify changes to the transcriptome in response to the QD. RT-qPCR assay was performed to confirm the findings of transcriptome analysis, and the QD mode of action was illustrated. Our study determined both IC50 concentration of 69 µg/mL and MIC concentration of 167 µg/mL of InP/ZnS. It was observed via XTT assay that cell viability was decreased significantly at the MIC. Production of superoxide, measured by ROS assay with flow cytometry, was decreased, whereas levels of nitrogen radicals increased. Using analysis of apoptosis, we found that induced cell death in the QD-treated samples was shown to be significantly increased when compared to untreated cells. We conclude InP/ZnS QD to decrease cell viability by inducing stress via ROS levels, apoptosis induction, and alteration of transcriptome.

Quantum dots are nanoparticles (2–10 nm) that emit strong and tunable fluorescence. Quantum dots have been heavily used in high-demand commercialized products, research, and for medical purposes. Emerging concerns have demonstrated the negative impact of quantum dots on living cells; however, the intracellular trafficking of QDs in yeast cells and the effect of this interaction remains unclear. The primary goal of our research is to investigate the trafficking path of red cadmium selenide zinc sulfide quantum dots (CdSe/ZnS QDs) in Saccharomyces cerevisiae and the impact QDs have on yeast cellular dynamics. Using cells with GFP-tagged reference organelle markers and confocal microscopy, we were able to track the internalization of QDs. We found that QDs initially aggregate at the exterior of yeast cells, enter the cell using clathrin-receptor-mediated endocytosis, and distribute at the late Golgi/trans-Golgi network. We also found that the treatment of red CdSe/ZnS QDs resulted in growth rate reduction and loss of polarized growth in yeast cells. Our RNA sequence analysis revealed many altered genes. Particularly, we found an upregulation of DID2, which has previously been associated with cell cycle arrest when overexpressed, and a downregulation of APS2, a gene that codes for a subunit of AP2 protein important for the recruitment of proteins to clathrin-mediated endocytosis vesicle. Furthermore, CdSe/ZnS QDs treatment resulted in a slightly delayed endocytosis and altered the actin dynamics in yeast cells. We found that QDs caused an increased level of F-actin and a significant reduction in profilin protein expression. In addition, there was a significant elevation in the amount of coronin protein expressed, while the level of cofilin was unchanged. Altogether, this suggests that QDs favor the assembly of actin filaments. Overall, this study provides a novel toxicity mechanism of red CdSe/ZnS QDs on yeast actin dynamics and cellular processes, including endocytosis.

Quantum dots (QDs) are a type of nanoparticle with excellent optical properties, suitable for many optical-based biomedical applications. However, the potential of quantum dots to be used in clinical settings is limited by their toxicity. As such, much effort has been invested to examine the mechanism of QDs’ toxicity. Yet, the current literature mainly focuses on ROS- and apoptosis-mediated cell death induced by QDs, which overlooks other aspects of QDs’ toxicity. Thus, our study aimed to provide another way by which QDs negatively impact cellular processes by investigating the possibility of protein structure and function modification upon direct interaction. Through shotgun proteomics, we identified a number of QD-binding proteins, which are functionally associated with essential cellular processes and components, such as transcription, translation, vesicular trafficking, and the actin cytoskeleton. Among these proteins, we chose to closely examine the interaction between quantum dots and actin, as actin is one of the most abundant proteins in cells and plays crucial roles in cellular processes and structural maintenance. We found that CdSe/ZnS QDs spontaneously bind to G-actin in vitro, causing a static quenching of G-actin’s intrinsic fluorescence. Furthermore, we found that this interaction favors the formation of a QD–actin complex with a binding ratio of 1:2.5. Finally, we also found that CdSe/ZnS QDs alter the secondary structure of G-actin, which may affect G-actin’s function and properties. Overall, our study provides an in-depth mechanistic examination of the impact of CdSe/ZnS QDs on G-actin, proposing that direct interaction is another aspect of QDs’ toxicity.