Protein corona exacerbated inflammatory response in macrophages elicited by CdTe quantum dots.

Nano-bio interface is significant concern in nanomedicine. When nanoparticles (NPs) come into contact with cells, they form complexes with proteins known as protein corona (PC). Cadmium telluride quantum dots (CdTe QDs) have been applied as bioimaging probes and for macrophage theragnostic. However, the impact of protein corona on the behavior of CdTe QDs is not well understood. Macrophages play a crucial role in defending against NPs. In this study, RAW264.7 cells were used to investigated the inflammatory response in macrophages when exposed to CdTe QDs before and after PC formation in fetal bovine serum. The results indicated that protein corona polarized more macrophages towards M1 phenotype. Transcriptomics analysis revealed that PC-CdTe QDs altered a greater number of differentially expressed genes (DEGs) compared to CdTe QDs (177 and 398) at 1.0 µM in macrophages. The DEGs affected by PC-CdTe QDs contained several personalized inflammatory cytokines. The enriched pathways after PC formation included Cytokine-cytokine receptor interaction, NOD-like receptor signaling pathway, and TNF signaling pathway, etc. Furthermore, PC specifically exacerbated the overexpression of CCL2 and IL-1ß proteins. Importantly, PC altered the mechanism of CdTe QD-induced pyroptosis, shifting it from activating NLRC4 to both NLRP1 and NLRP3 inflammasomes, and from cleaving GSDMD and GSDMB to GSDMB alone. Overall, protein corona exacerbated the inflammatory response induced by CdTe QDs in macrophages. This study provides valuable insight into the pro-inflammatory effect of protein corona on CdTe QDs, with implications for their use in bioimaging or macrophage theragnostic by either exploiting or eliminating this biological interface effect.

Application of Se-Met to CdTe QDs significantly reduces toxicity by modulating redox balance and inhibiting apoptosis.

Cadmium tellurium quantum dots (CdTe QDs) as one of the most widely used QDs have been reported the toxicity and biosafety in recent years, little work has been done to reduce their toxicity however. Based on the mechanisms of toxicity of CdTe QDs on liver target organs such as oxidative stress and apoptosis previously reported by other researchers, we investigated the mechanism of action of trace element selenium (Se) to mitigate the hepatotoxicity of CdTe QDs. The experimental results showed that Se-Met at 40-140 µg L-1 could enhance the function of intracellular antioxidant defense system and the molecular structure of related antioxidant enzymes by reduce the production of ROS by 45%, protecting the activity of antioxidants and up-regulating the expression of selenoproteins with antioxidant functions, Gpx1 increase 225% and Gpx4 upregulated 47%. In addition, Se-Met could alleviate CdTe QDs-induced apoptosis by regulating two apoptosis-inducing factors, as intracellular caspase 3/9 expression levels were reduced by 70% and 87%, decreased Ca2+ concentration, and increased mitochondrial membrane potential measurements. Overall, this study indicates that Se-Met has a significant protective effect on the hepatotoxicity of CdTe QDs. Se-Met can be applied to the preparation of CdTe QDs to inhibit its toxicity and break the application limitation.

MPA-capped CdTequantum dots induces endoplasmic reticulum stress-mediated autophagy and apoptosis through generation of reactive oxygen species in human liver normal cell and liver tumor cell.

The rapid developments in nanotechnology have brought increased attention to the safety of Quantum Dots (QDs). Exploring their mechanisms of toxicity and characterizing their toxic effects in different cell lines will help us better understand and apply QDs appropriately. This study aims to elucidate the importance of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress-induced autophagy for CdTe QDs toxicity, that is, the importance of the nanoparticles in mediating cellular uptake and consequent intracellular stress effects inside the cell. The results of the study showed that cancer cells and normal cells have different cell outcomes as a result of intracellular stress effects. In normal human liver cells (L02), CdTe QDs leads to ROS generation and prolong ER stress. The subsequent autophagosome accumulation eventually triggers apoptosis by activating proapoptotic signaling pathways and the expression of proapoptotic Bax. In contrast, in human liver cancer cells (HepG2 cells), expression of UPR restrains proapoptotic signaling and downregulates Bax, and activated protective cellular autophagy, as a result of protecting these liver cancer cells from CdTe QDs-induced apoptosis. In summary, we assess the safety of CdTe QDs and recounted the molecular mechanism underlying its nanotoxicity in normal and cancerous cells. Notwithstanding, additional detailed studies on the deleterious effects of these nanoparticles in the organisms of interest are required to ensure low-risk application.

CdTe quantum dots trigger oxidative stress and endoplasmic reticulum stress-induced apoptosis and autophagy in rat Schwann cell line RSC96.

In the current study, the cytotoxicity and mechanisms of cadmium telluride quantum dots (CdTe QDs) on RSC96 cells were evaluated by exposing different doses of CdTe QDs for 24 h. Two types of cell death, including apoptosis and autophagy, as well as two important organelles, mitochondria and endoplasmic reticulum, were focused after CdTe QDs exposure. The results showed that CdTe QDs induced apoptosis in RSC96 cells in a concentration-dependent manner; promoted the accumulation of intracellular reactive oxygen species; decreased the mitochondrial membrane potential; caused the release of cytochrome c; and also increased the expression of Bcl-2 associated X protein, caspase-3, and cytochrome c proteins and decreased the expression of Bcl-2 protein. Further results also confirmed that CdTe QDs could be internalized by RSC96 cells, and the exposure and internalization of CdTe QDs could induce excessive endoplasmic reticulum stress in the cells, and the expression levels of binding immunoglobulin protein, C/EBP homologous protein, and caspase12 proteins were increased in a concentration-dependent manner. Moreover, autophagy-related proteins LC3II, Beclin1, and P62 all increased after CdTe QDs exposure, suggesting that CdTe QDs exposure both promoted autophagosome formation and inhibited autophagosome degradation, and that CdTe QDs affected the autophagic flow in RSC96 cells. In conclusion, CdTe QDs are able to cause apoptosis and autophagy in RSC96 cells through mitochondrial and endoplasmic reticulum stress pathways, and the possible neurotoxicity of CdTe QDs should be further investigated.

The role of ferroptosis mediated by NRF2/ERK-regulated ferritinophagy in CdTe QDs-induced inflammation in macrophage.

Cadmium telluride quantum dots (CdTe QDs) exist in the environment due to the abandonment of products. There is a potential risk to organisms and toxic mechanism is worth exploring. In this study, 12.5 µmol/Kg body weight CdTe QDs triggered systemic and local inflammatory response in mice and activated macrophages, then the mechanism of activating macrophages to overexpress IL-1ß and IL-6 was explored. RAW264.7 macrophages were used, and after macrophages exposing to 1 µM CdTe QDs for 24 h, oxidative stress occurred. Further investigation found that CdTe QDs triggered ferroptosis in RAW264.7 cells. And deferoxamine mesylate alleviated the excessive lipid hydroperoxide caused by QDs. Mechanistically, CdTe QDs-provoked decrease of nuclear factor erythroid 2-related factor 2 (NRF2) elicited phosphorylation of extracellular regulated protein kinases1/2 (ERK1/2) and then activated ferritinophagy, which made ferritin heavy chain 1 (FTH1) degraded in lysosome and proteasome to release free iron ions to initiate ferroptosis in macrophages. This paper updates the mechanism of macrophage activation by CdTe QDs with regard to ferritinophagy, and more importantly, identifies the key role of NRF2 and ERK1/2. Our research extends the role of ferroptosis in inflammatory responses triggered by nanoparticles (NPs) in macrophages and provides insightful reference for toxicity assessment of NPs.

Intracellular reactive oxygen species trigger mitochondrial dysfunction and apoptosis in cadmium telluride quantum dots-induced liver damage.

Quantum dots (QDs), also known as semiconductor QDs, have specific photoelectricproperties which find application in bioimaging, solar cells, and light-emitting diodes (LEDs). However, the application of QDs is often limited by issues related to health risks and potential toxicity. The purpose of this study was to provide evidence regarding the safety of cadmium telluride (CdTe) QDs by exploring the detailed mechanisms involved in its hepatotoxicity. This study showed that CdTe QDs can increase reactive oxygen species (ROS) in hepatocytes after being taken up by hepatocytes, which triggers a significant mitochondrial-dependent apoptotic pathway, leading to hepatocyte apoptosis. CdTe QDs-induce mitochondrial cristae abnormality, adenosine triphosphate (ATP) depletion, and mitochondrial membrane potential (MMP) depolarization. Meanwhile, CdTe QDs can change the morphology, function, and quantity of mitochondria by reducing fission and intimal fusion. Importantly, inhibition of ROS not only protects hepatocyte viability but can also interfere with apoptosis and activation of mitochondrial dysfunction. Similarly, the exposure of CdTe QDs in Institute of Cancer Research (ICR) mice showed that CdTe QDs caused oxidative damage and apoptosis in liver tissue. NAC could effectively remove excess ROS could reduce the level of oxidative stress and significantly alleviate CdTe QDs-induced hepatotoxicity in vivo. CdTe QDs-induced hepatotoxicity may originate from the generation of intracellular ROS, leading to mitochondrial dysfunction and apoptosis, which was potentially regulated by mitochondrial dynamics. This study revealed the nanobiological effects of CdTe QDs and the intricate mechanisms involved in its toxicity at the tissue, cell, and subcellular levels and provides information for narrowing the gap between in vitro and in vivo animal studies and a safety assessment of QDs.

Protein corona mitigated the cytotoxicity of CdTe QDs to macrophages by targeting mitochondria.

Despite the potential of cadmium telluride quantum dots (CdTe QDs) in bioimaging and drug delivery, their toxic effects have been documented. It is known that the immunotoxicity of CdTe QDs targeting macrophages is one of their adverse effects, and the protein corona (PC) will affect the biological effects of QDs. In order to prove whether the PC-CdTe QDs complexes could alleviate the toxicity of CdTe QDs without weakening their luminescence, we investigated the impact of protein corona formed in fetal bovine serum (FBS) on the cytotoxicity of CdTe QDs to mitochondria. RAW264.7 cells were used as the model to compare the effects of CdTe QDs and PC-CdTe QDs complexes on the structure, function, quantity, morphology, and mitochondrial quality control of mitochondria. As result, the protein corona form in FBS alleviated the inhibition of CdTe QDs on mitochondrial activity, the damage to mitochondrial membrane, the increase of ROS, and the reduction of ATP content. Also, CdTe QDs increased the number of mitochondria in macrophages, while the complexes did not. In line with this, the morphology of mitochondrial network in macrophages which were exposed to CdTe QDs and PC-CdTe QDs complexes was different. CdTe QDs transformed the network into fragments, punctuations, and short rods, while PC-CdTe QDs complexes made the mitochondrial network highly branched, which was related to the imbalance of mitochondrial fission and fusion. Mechanically, CdTe QDs facilitated mitochondrial fission and inhibited mitochondrial fusion, while protein corona reversed the phenomenon caused by QDs. Besides mitochondrial dynamics, mitochondrial biogenesis and mitophagy were also affected. CdTe QDs increased the expression of mitochondrial biogenesis signaling molecules including PGC-1α, NRF-1 and TFAM, while PC-CdTe QDs complexes played the opposite role. With regard to mitophagy, they both showed promoting effect. In conclusion, the formation of protein corona alleviated the toxic effects of CdTe QDs on the mitochondria in macrophages and affected mitochondrial quality control. Under the premise of ensuring the fluorescence properties of CdTe QDs, these findings provided useful insight into reducing the toxicity of CdTe QDs from two perspectives: protein corona and mitochondria, and shared valuable information for the safe use of QDs.

Mechanism of ER stress-mediated ER-phagy by CdTe-QDs in yeast cells.

Endoplasmic reticulum autophagy (ER-phagy) is an important strategy for cells against ER stress and maintain ER homeostasis. ER stress is considered as a potential toxicity of nanoparticles, but only a few studies have explored whether the nanoparticles-induced ER stress can trigger ER-phagy, and the precise molecular mechanism of ER-phagy mediated by nanoparticle-induced ER stress is still poorly understood. Therefore, our study focuses on the relationship between ER stress and ER-phagy caused by emerging nanoparticles CdTe-QDs and its molecular mechanism. The results showed that the accumulation of ROS and ER stress induced by CdTe-QDs contributed to the activation of autophagy and ER-phagy. Importantly, our study unraveled that CdTe-QDs activate autophagy by up-regulating the transcription of core autophagy machinery. It was found that the induced ER-phagy was mediated by Atg11/Atg40/Lst1-Sec23 instead of the autophagy machinery genes. We speculated that the ER-phagy caused by CdTe-QDs may include micro-ER-phagy and macro-ER-phagy. Collectively, this work provided valuable information for the application of CdTe-QDs in the field of biology and a theoretical basis for further understanding of ER-phagy.

Dysbiosis of gut microbiota and intestinal damage in mice induced by a single intravenous exposure to CdTe quantum dots at low concentration.

Although quantum dots (QDs) have shown great potential for various biomedical applications, their potential toxicity still needs to be comprehensively investigated. Previous studies showed that intravenous exposure of CdTe QDs at low concentration did not lead to obvious in vivo toxicity in the long term. However, the influence of CdTe QDs on the gut microbiota and the intestine is still unknown. Here, we explored whether single intravenous injection of CdTe QDs at low concentration can affect the gut microbiota and intestine of mice in short term. The results showed that CdTe QDs caused an imbalance of gut microbiota, especially the rapid increase in Lactobacillus on day 1 post-treatment. Meanwhile, the intestine exhibited the promotion of oxidative stress, inflammatory response, and hemorrhaging on days 5 and 15. These results demonstrate that the gut microbiota and the intestine are very sensitive to the toxicity of low-concentration CdTe QDs. This study provides further insight and method for the biosafety evaluation of nanomaterials.

Systematic toxicity assessment of CdTe quantum dots in Drosophila melanogaster.

The risk assessment of cadmium (Cd)-based quantum dots (QDs) used for biomedical nanotechnology applications has stern toxicity concerns. Despite cytotoxicity studies of cadmium telluride (CdTe) QDs, the systematic in vivo study focusing on its organismal effects are more relevant to public health. Therefore, the present study aims to investigate the effect of chemically synthesized 3-mercapto propionic acid-functionalized CdTe QDs on organisms' survival, development, reproduction, and behaviour using Drosophila melanogaster as a model. The sub-cellular impact on the larval gut was also evaluated. First/third instar larvae or the adult Drosophila were exposed orally to green fluorescence emitting CdTe QDs (0.2-100 µM), and organisms' longevity, emergence, reproductive performance, locomotion, and reactive oxygen species (ROS), and cell death were assessed. Uptake of semiconductor CdTe QDs was observed as green fluorescence in the gut. A significant decline in percentage survivability up to 80% was evident at high CdTe QDs concentrations (25 and 100 µM). The developmental toxicity was marked by delayed and reduced fly emergence after CdTe exposure. The teratogenic effect was evident with significant wing deformities at 25 and 100 µM concentrations. However, at the reproductive level, adult flies' fecundity, fertility, and hatchability were highly affected even at low concentrations (1 µM). Surprisingly, the climbing ability of Drosophila was unaffected at any of the used CdTe QDs concentrations. In addition to organismal toxicity, the ROS level and cell death were elevated in gut cells, confirming the sub-cellular toxicity of CdTe QDs. Furthermore, we observed a significant rescue in CdTe QDs-associated developmental, reproductive, and survival adversities when organisms were co-exposed with N-acetyl-cysteine (NAC, an antioxidant) and CdTe QDs. Overall, our findings indicate that the environmental release of aqueously dispersible CdTe QDs raises a long-lasting health concern on the development, reproduction, and survivability of an organism.

Induction of autophagy and endoplasmic reticulum autophagy caused by cadmium telluride quantum dots are protective mechanisms of yeast cell.

Quantum dots (QDs), with unique and tunable optical properties, have been widely used in many fields closely related to our daily lives, such as biomedical application and electronic products. Therefore, the potential toxicity of QDs on the human health should be understood. Autophagy plays an important role in cell survival and death. Endoplasmic reticulum autophagy (ER-phagy), a selective autophagy that degrades ER, responds to the accumulation of misfolded proteins and ER stress. Although many reports have revealed that autophagy can be disturbed by cadmium telluride (CdTe)-QDs and other nanomaterials, there are still lack more detailed researches to illustrate the function of autophagy in CdTe-QDs-treated cells, and the function of ER-phagy in CdTe-QDs-treated cells remains to be illustrated. On the basis of transcriptome analysis, we explored the effect of CdTe-QDs on Saccharomyces cerevisiae and first illustrated that both of autophagy and ER-phagy were protective mechanisms in CdTe-QDs-treated cells. It was found that CdTe-QDs inhibited the proliferation of yeast cells, disrupted homeostasis of cells, membrane integrity, and metabolism process. All of these can be reasons of the reduction of cell viability. The abolishment of autophagy and ER-phagy reduce the cell survival, indicating both of them are cell protective mechanisms against CdTe-QDs toxicity in yeast cells. Therefore, our data are significant for the application of CdTe-QDs and provide precious information for understanding of nanomaterials-related ER-phagy.

The apoptosis induced by CdTe quantum dots through the mitochondrial pathway in dorsal root ganglion cell line ND7/23.

Recently, the use of CdTe quantum dots in the field of biomedicine, such as biological imaging, biosensors, cell markers, and drug carriers, is increasing due to their special physical and chemical properties. However, their biosafety assessment lags far behind their rapid application. In this study, we observed that CdTe quantum dots with certain exposed doses and time decreased the cell viability and increased the apoptosis rates in ND7/23 cells. In general, CdTe quantum dots exposure could promote the accumulation of reactive oxygen species (ROS) in cells and decrease the mitochondrial membrane potential, which led to pathological changes and subcellular organelle damages. We hypothesized that the mitochondrial pathway could be involved in CdTe quantum dots-induced apoptosis. The results suggested that CdTe quantum dots exposure increased the expression levels of three mitochondrial pathway markers, for example, caspase-3, cytochrome c, and Bax while decreased Bcl-2 protein expression, following with cytochrome c falling out of the inner membrane of mitochondrial and releasing into the cytoplasm. The application of caspase-3 protein inhibitor Ac-DEVD-CHO could decrease apoptosis rates in ND7/23 cells. The results, taken together, demonstrated that CdTe quantum dots could induce apoptosis of ND7/23 cells through the mitochondrial pathway. Our findings provide a novel insight for researchers to explore CdTe quantum dots' toxic mechanisms to reduce their adverse effects.

Reactive oxygen species trigger NF-κB-mediated NLRP3 inflammasome activation involvement in low-dose CdTe QDs exposure-induced hepatotoxicity.

Cadmium telluride (CdTe) quantum dots (QDs) can be employed as imaging and drug delivery tools; however, the toxic effects and mechanisms of low-dose exposure are unclear. Therefore, this pioneering study focused on hepatic macrophages (Kupffer cells, KCs) and explored the potential damage process induced by exposure to low-dose CdTe QDs. In vivo results showed that both 2.5 µM/kg·bw and 10 µM/kg·bw could both activate KCs to cause liver injury, and produce inflammation by disturbing antioxidant levels. Abnormal liver function further verified the risks of low-dose exposure to CdTe QDs. The KC model demonstrated that low-dose CdTe QDs (0 nM, 5 nM and 50 nM) can be absorbed by cells and cause severe reactive oxygen species (ROS) production, oxidative stress, and inflammation. Additionally, the expression of NF-κB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-κB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 µg/mL pretreatment for 4 h) respectively. The results indicate that the activation of the NF-κB pathway by ROS not only directly promotes the expression of inflammatory factors such as pro-IL-1ß, TNF-α, and IL-6, but also mediates the assembly of NLRP3 by ROS activation of NF-κB pathway, which indirectly promotes the expression of NLRP3. Finally, a high-degree of overlap between the expression of the NF-κB and NLRP3 and the activated regions of KCs, further support the importance of KCs in inflammation induced by low-dose CdTe QDs.

Bioaccessibility as a determining factor in the bioavailability and toxicokinetics of cadmium compounds.

Cadmium toxicity occurs where there is absorption and accumulation of cadmium ions (Cd2+) in tissues beyond tolerable levels. Significant differences in the release of Cd2+ from cadmium compounds in biological fluids, like gastric fluid, may indicate differences in bioavailability and absorption. This means that direct read-across from high solubility cadmium compounds to lower solubility compounds may not accurately reflect potential hazards. Here, the relative bioaccessibility in gastric fluid of cadmium telluride and cadmium chloride was evaluated using in vitro bioelution tests whilst the toxicokinetic behavior of these two compounds were compared after dietary administration for 90 days in male and female Wistar Han rats following OECD TG 408. Cadmium chloride was highly bioaccessible, whilst cadmium telluride showed low solubility in simulated gastric fluid (90 % and 1.5 % bioaccessibility, respectively). This difference in bioaccessibility was also reflected by a difference in bioavailability as shown by the difference in the liver and kidney concentrations of cadmium after repeat oral exposure. Feeding at doses of 750 and 1500 ppm of cadmium telluride did not result in tissue cadmium levels above the lower limit of quantification (LLOQ). In contrast, feeding with a lower test substance concentration yet higher concentration of bioaccessible cadmium (30 ppm cadmium chloride) resulted in tissue accumulation of cadmium. Only slight, non-adverse changes in hematology and clinical chemistry parameters were seen at these doses, indicating an absence of significant cadmium mediated toxicity towards target organs (kidney and liver), reflected in minimal cadmium accumulation in these organs. This study demonstrates that bioelution tests can help determine the bioaccessibility of cadmium, which can be used to estimate the potential for target tissue toxicity based on known toxicokinetic profiles and threshold levels for cadmium toxicity, while reducing and refining animal testing.

Investigating the interaction of CdTe quantum dots with plasma protein transferrin and their interacting consequences at the molecular and cellular level.

This study investigated the interacting mechanism of CdTe quantum dots (QDs) with typical plasma protein transferrin (TF) as well as the impact of the formation of QDs-TF complex on the structure of TF and the cytotoxicity of mouse primary kidney cells. Dialysis experiments and cell viability assays revealed that the formation of QDs-TF complex reduced the contents of Cd released from CdTe QDs and thus counteracted the cytotoxicity of CdTe QDs. The assay of isothermal titration calorimetry found that CdTe QDs complexed with TF majorly through hydrophobic interaction. Multi-spectroscopic measurements showed that CdTe QDs caused the loosening of polypeptide chain, the changes of secondary and tertiary structures as well as the attenuated aggregation of TF molecule. Moreover, these structural and conformational changes were attributed to the nano-effects of CdTe QDs rather than the released Cd. This study is of great significance for fully evaluating the biocompatibility of Cd-QDs and comprehensively understanding the mechanism of Cd-QDs toxicity at the molecular and cellular level.

Involvement of nitrosative stress cytotoxicity induced by CdTe quantum dots in human vascular endothelial cells.

Quantum dots (QDs) are new types of fluorescent nanomaterials which can be utilized as ideal agents for intracellular tracking, drug delivery, biomedical imaging and diagnosis. It is urgent to understand their potential toxicity and the interactions with the toxin-susceptible vascular system, especially vascular endothelial cells. In this study, we intended to explore whether the cytotoxicity of CdTe (cadmium telluride) QDs was partly induced by nitrosative stress in vascular endothelial cells. Our results showed that the intracellular amount of CdTe QDs was gradually increased in a dose- and time-dependent manner, and a concentration-dependent decrease in viability were observed when incubated with CdTe QDs of 20-80 nM. The peroxynitrite level was significantly up-regulated by QDs treatment, which indicated the nitrosative stress was activated. Furthermore, nitrotyrosine level was increased after 24 hr CdTe QDs exposure in a dose-dependent manner, which suggested that CdTe QDs-induced nitrosative stress was associated with tyrosine nitration in EA.hy926. In addition, CdTe QDs induced EA.hy926 apoptosis, and the percentage of cells with low Δψm was increased after CdTe QDs treatment, indicating the mitochondrion depolarization was induced. The increased ROS fluorescence was observed in a QDs dose-dependent manner, which suggested that the oxidative stress was also involved in the CdTe QDs-induced endothelial cytotoxicity. Our work provided experimental evidence into QDs toxicity and potential vascular risks induced by nitrosative stress for the future applications of QDs.

Tellurium: A Rare Element with Influence on Prokaryotic and Eukaryotic Biological Systems.

Metalloid tellurium is characterized as a chemical element belonging to the chalcogen group without known biological function. However, its compounds, especially the oxyanions, exert numerous negative effects on both prokaryotic and eukaryotic organisms. Recent evidence suggests that increasing environmental pollution with tellurium has a causal link to autoimmune, neurodegenerative and oncological diseases. In this review, we provide an overview about the current knowledge on the mechanisms of tellurium compounds' toxicity in bacteria and humans and we summarise the various ways organisms cope and detoxify these compounds. Over the last decades, several gene clusters conferring resistance to tellurium compounds have been identified in a variety of bacterial species and strains. These genetic determinants exhibit great genetic and functional diversity. Besides the existence of specific resistance mechanisms, tellurium and its toxic compounds interact with molecular systems, mediating general detoxification and mitigation of oxidative stress. We also discuss the similarity of tellurium and selenium biochemistry and the impact of their compounds on humans.

1T-Phase Dirac Semimetal PdTe2 Nanoparticles for Efficient Photothermal Therapy in the NIR-II Biowindow.

1T-phase transition-metal dichalcogenides (TMDs) nanomaterials are one type of emerging and promising near-infrared II (NIR-II) photothermal agents (PTAs) derived from their distinct metallic electronic structure, but it is still challenging to synthesize these nanomaterials. Herein, PdTe2 nanoparticles (PTNs) with a 1T crystal symmetry and around 50 nm in size are prepared by an electrochemical exfoliation method, and the corresponding photothermal performances irradiated under a NIR-II laser have been explored. The encapsulation of 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-poly(ethylene glycol) (DSPE-PEG) endows PTNs with water solubility, enhanced photothermal stability, and high biocompatibility. Notably, PTN/DSPE-PEG displays a potent absorbance through the NIR-II zone and considerable photothermal conversion efficiency, which is up to 68% when irradiated with a 1060 nm laser. With these unique photothermal properties, excellent in vitro and in vivo tumor inhibition effects of PTN/DSPE-PEG have been achieved under the irradiation of a NIR-II (1060 nm) laser without visible toxicity to normal tissues, suggesting that it is an efficient NIR-II photothermal nanoagent.

Release and cytotoxicity screening of the printer emissions of a CdTe quantum dots-based fluorescent ink.

The fluorescent properties of cadmium telluride (CdTe) containing quantum dots (QDs) have led to novel products and applications in the ink and pigment industry. The toxic effects of the emissions associated to the use of printing ink containing CdTe QDs might differ from those of conventional formulations which do not integrate nanoparticles, as CdTe QDs might be emitted. Within this work, the airborne emissions of a water-soluble fluorescent ink containing polyethylene glycol (PEG)-coated CdTe QDs of 3-5 nm diameter have been characterized and studied under controlled conditions during household inkjet printing in a scenario simulating the use phase. Subsequently, the cytotoxicological potential of atomized CdTe QDs ink in an acute exposure regimen simulating an accidental, worse-case scenario has been evaluated in vitro at the air-liquid interface (ALI) using the pulmonary cell line BEAS-2B. Endpoints screened included cell viability, oxidative stress and inflammatory effects. We have observed that CdTe QDs ink at 54.7 ng/mL decreased cell viability by 25.6 % when compared with clean air after 1h of exposure; a concentration about 65 times higher was needed to observe a similar effect in submerged conditions. However, we did not observe oxidative stress or inflammatory effects. The present study integrates the development of scenarios simulating the use phase of nano-additivated inks and the direct cell exposure for in vitro effects assessment, thus implementing a life-cycle oriented approach in the assessment of the toxicity of CdTe QDs.

Toxicity evaluation of cadmium-containing quantum dots: A review of optimizing physicochemical properties to diminish toxicity.

Fluorescent quantum dots (QDs) have received extensive attention because of their excellent optical properties and wide utilization in biological and biomedical areas. Nonetheless, there have been intense concerns on the cytotoxicity assessment of cadmium-containing QDs due to free cadmium ions release and nano-size effects. This paper reviews the representative synthetic strategies for preparation of cadmium-containing QDs and their applications. Then the toxicity assessments of QDs from cell studies to animal models are discussed, which can aid in improving our understanding of the cytotoxicity of QDs, and the toxicity mechanism is proposed. Several critical physicochemical properties of QDs are discussed and suggestions are provided for optimizing QDs design in view of minimal cytotoxicity. Finally, accurate detection techniques and systematic methodologies for the toxicity assessment of QDs are expected to achieve further breakthroughs in the future, especially in-situ, real-time, and rapid quantitative analysis methods.