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Tellurium (Te) is a metalloid widely used in various industries. However, its toxicological impact on humans is poorly understood. In this study, we investigated the role of two methyltransferases, thiopurine S‑methyltransferase (TPMT) and indolethylamine N‑methyltransferase (INMT), in the methylation of tellurite, an inorganic Te oxyanion. The products of the reaction of Te compounds catalyzed by recombinant human TPMT and/or INMT were analyzed by liquid chromatography hyphenated to inductively coupled plasma mass spectrometry (LC-ICP-MS) and gas chromatography mass spectrometry (GC-MS). We found that TPMT catalyzes the methylation of non-methylated Te and methanetellurol to generate dimethyltelluride. On the other hand, INMT catalyzes the methylation of methanetellurol and dimethyltelluride to produce trimethyltelluronium ion, a metabolite excreted into animal urine. We conclude that TPMT and INMT are cooperatively responsible for the detoxification of Te oxyanions through methylation to form trimethyltelluronium ions., Competing Interests: Declarations. Conflict of interests: The authors declare no conflicts of interest., (© 2024. The Author(s).)

Cadmium telluride (CdTe) quantum dots (QDs) have garnered significant attention for tumor imaging due to their exceptional properties. However, there remains a need for further investigation into their potential toxicity mechanisms and corresponding enhancements. Herein, CdTe QDs were observed to accumulate in mouse liver, leading to a remarkable overproduction of IL-1β and IL-6. Additionally, there was evidence of macrophage infiltration and activation following exposure to 12.5 μmol/kg body weight of QDs. To elucidate the underlying mechanism of macrophage activation, CdTe QDs functionalized with 3-mercaptopropionic acid (MPA) were utilized. In vitro experiments revealed that 1.0 μM MPA-CdTe QDs activated PINK1-dependent mitophagy in RAW264.7 macrophages. Critically, the autophagic flux remained unimpeded, as demonstrated by the absence of p62 accumulation, LC3 turnover assay results, and successful fusion of autophagosomes with lysosomes. Mechanically, QDs increased reactive oxygen species (ROS) and mitoROS by damaging both mitochondria and lysosomes. ROS, in turn, inhibited NRF2, resulting in the phosphorylation of ERK1/2 and subsequent activation of mitophagy. Notably, 1.0 μM QDs disrupted lysosomes but autophagic flux was not impaired. Eventually, the involvement of the ROS-NRF2-ERK1/2 pathway-mediated mitophagy in the increase of IL-1β and IL-6 in macrophages was confirmed using Trolox, MitoTEMPO, ML385, specific siRNAs, and lentivirus-based interventions. This study innovatively revealed the pro-inflammatory rather than anti-inflammatory role of mitophagy in nanotoxicology, shedding new light on the mechanisms of mitochondrial disorders induced by QDs and identifying several molecular targets to comprehend the toxicological mechanisms of CdTe QDs., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The development of antibiotic resistance and the onset of diverse forms of cancer necessitate the utilization of innovative multifunctional biocompatible materials. The synthesis of metal and metalloid nanoparticles through eco-friendly means demonstrates promising potential in therapeutic and diagnostic domains. Among these materials, Tellurium (Te) exhibits exceptional characteristics and finds application in numerous fields; nevertheless, its usage in biological applications has been somewhat limited, primarily due to its inherent toxicity. Furthermore, nanomaterials developed from Te have not garnered adequate research attention. Conversely, nanomaterials fashioned using biomolecules augment their biological efficacy and applicability. Therefore, the present work focuses on synthesizing the tellurium nanoparticles (Te NPs) using the antioxidant molecule gallic acid (GA) and evaluating their biological activity and toxicity for the first time. The study evidenced that GA-Te NPs are spherical and monodispersed, with an average size of 19.74 ± 5.3 nm. XRD analysis confirmed a hexagonal crystalline structure for GA-Te NPs, and FTIR analysis evidenced the capping of GA on Te NPs. GA-Te NPs (MIC: 1.56 μg/mL) strongly reduce the growth and biofilm formation of S. aureus, E. coli, and S. enterica. Additionally, GA-Te NPs at a concentration of 50 μg/mL cause a significant level of toxicity in BT474 breast cancer cells but not in NIH3T3 cells. Unexpectedly, GA-Te NPs at concentrations <250 μg/mL do not cause hemolysis in red blood cells (RBC) Besides, the way of utilizing the lower concentrations of therapeutics could result in ecological safety. Therefore, the study concludes that GA-Te NPs could be used as potential multifunctional agents., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

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-1β 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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 Ca 2+ 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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

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., (© 2022 John Wiley & Sons Ltd.)

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., (© 2022 John Wiley & Sons, Ltd.)

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-1β 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., (Copyright © 2022 Elsevier B.V. All rights reserved.)

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., (Copyright © 2022. Published by Elsevier B.V.)

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., (© 2022 John Wiley & Sons, Ltd.)

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., (© 2022 John Wiley & Sons, Ltd.)

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., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

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., (Copyright © 2022 Elsevier B.V. All rights reserved.)

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., (Copyright © 2021. Published by Elsevier B.V.)

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-1β, 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., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Cadmium toxicity occurs where there is absorption and accumulation of cadmium ions (Cd 2+ ) in tissues beyond tolerable levels. Significant differences in the release of Cd 2+ 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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

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., Competing Interests: Declaration of Competing Interest The authors report no declarations of interest., (Copyright © 2021. Published by Elsevier B.V.)

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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

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, PdTe 2 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.

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.

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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Quantum dots (QDs) are nanoparticles of inorganic semiconductors and have great promise in various applications. Many studies have indicated that mitochondria are the main organelles for the distribution and toxic effects of QDs. However, the underlying mechanism of QDs interacting with mitochondria and affecting their function is unknown. Here, we report the mechanism of toxic effects of 3-mercaptopropionic acid (MPA)-capped CdTe QDs on mitochondria. Human liver carcinoma (HepG2) cells were exposed to 25, 50 and 100 μmol/L of MPA-capped CdTe QDs. The results indicated that MPA-capped CdTe QDs inhibited HepG2 cell proliferation and increased the extracellular release of LDH in a concentration-dependent manner. Furthermore, MPA-capped CdTe QDs caused reactive oxygen species (ROS) generation and cell damage through intrinsic apoptotic pathway. MPA-capped CdTe QDs can also lead to the destruction of mitochondrial cristae, elevation of intracellular Ca 2+ levels, decreased mitochondrial transmembrane potential and ATP production. Finally, we showed that MPA-capped CdTe QDs inhibited mitochondrial fission, mitochondrial inner membrane fusion and mitophagy. Taken together, MPA-capped CdTe QDs induced significant mitochondrial dysfunction, which may be caused by imbalanced mitochondrial fission/fusion and mitophagy inhibition. These findings provide insights into the regulatory mechanisms involved in MPA-capped CdTe QDs-induced mitochondrial dysfunction., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Proficient fluorescent-characteristics, cytotoxicity-behavior and antimicrobial-activity of near-infrared-emitting (NIR) CdTe quantum dots (QDs) were studied sumptuously as these QDs are having an excellence in deep-tissue dissemination of light. These, NIR-emitting QDs were synthesized using aqueous method, utilizing 3-mercaptopropionic-acid (3-MPA) as a stabilizer; it controls leakage of Cd and Te ions from CdTe QDs. However, encapsulation by polymers also prevents the same by seizing toxic consequence of prepared QDs which was confirmed from cytotoxicity studies. Therefore, easy modification according to biological environment of these encapsulated CdTe QDs can serve in bio imaging and distribution. Antimicrobial study investigated the toxic effects of QDs against bacterial strains and support cytotoxicity studies and showing maximum 26 mm zone of inhibition against bacterial strain. These, NIR fluorescent QDs possess many attractive optical properties over the standard fluorescent probes (organic dyes) and can replace these dyes, as there is no specific dye which works in NIR range., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Since nano-quantum dots (QDs) are increasingly used as fluorescent dyes in biomedical sciences, the possibility of QDs contaminating aquatic environments is generally increasing. There is concern about potential toxicity of QDs. However, their risks in the aquatic environment are not entirely understood. In this study, the freshwater crab Sinopotamon henanense was exposed to cadmium telluride (CdTe) QDs by intraperitoneal injection to detect the reproductive toxicity of QDs (1/32, 1/16 and 1/4 LD 50 ; Crab was exposed for 1, 3, 5, and 7 days). After CdTe QD exposure, no significant effect was detected on the body weight and gonadosomatic index. Additionally, morphological observations showed tissue vacuolation in the testis, and inflammatory cell infiltration in the ovary. The submicroscopic structure showed that exposure to CdTe QDs damaged the organelles and cell structures of the gonads of S. henanense. Among the adverse effects, pathological changes in the nuclear membrane, mitochondria and lysosomes were particularly significant. Antioxidant enzymes responded differently to different doses of QDs. The 0.5-mg/kg dose induced superoxide dismutase activity in the testes. And in the 1-mg/kg and 4-mg/kg dose QD exposure test, the testis responded by activating glutathione peroxidase and inducing reduced glutathione and overconsuming glutathione peroxidase. Respectively, the ovaries responded by overconsuming superoxide dismutase and glutathione peroxidase and reduced glutathione. Thus, we conclude that the gonads of S. henanense were injured by CdTe QD, and male are better indicators of the toxicity of QDs than female crabs according to greater alterations in tissue structure and antioxidant enzyme in the analyses., (Copyright © 2020. Published by Elsevier Inc.)

Tellurium oxyanions are chemical species of great toxicity and their presence in the environment has increased because of mining industries and photovoltaic and electronic waste. Recovery strategies for this metalloid that are based on micro-organisms are of interest, but further studies of the transport systems and enzymes responsible for implementing tellurium transformations are required because many mechanisms remain unknown. Here, we investigated the involvement in tellurite uptake of the putative phosphate transporter PitB (PP1373) in soil bacterium Pseudomonas putida KT2440. For this purpose, through a method based on the CRISPR/Cas9 system, we generated a strain deficient in the pitB gene and characterized its phenotype on exposing it to varied concentrations of tellurite. Growth curves and transmission electronic microscopy experiments for the wild-type and Δ pitB strains showed that both were able to internalize tellurite into the cytoplasm and reduce the oxyanion to black nano-sized and rod-shaped tellurium particles, although the Δ pitB strain showed an increased resistance to the tellurite toxic effects. At a concentration of 100 μM tellurite, where the biomass formation of the wild-type strain decreased by half, we observed a greater ability of Δ pitB to reduce this oxyanion with respect to the wild-type strain (~38 vs ~16 %), which is related to the greater biomass production of Δ pitB and not to a greater consumption of tellurite per cell. The phenotype of the mutant was restored on over-expressing pitB in trans . In summary, our results indicate that PitB is one of several transporters responsible for tellurite uptake in P. putida KT2440.

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.

The aim of this study was to investigate the detailed mechanisms of hepatotoxicity induced by cadmium telluride quantum dots (CdTe-QDs) in BALB/c mice after intravenous injection. The study investigated oxidative stress, apoptosis, and effects on mitochondria as potential mechanistic events to elucidate the observed hepatotoxicity. Oxidative stress in the liver, induced by CdTe-QD exposure, was demonstrated by depletion of total glutathione, an increase in superoxide dismutase activity, and changes in the gene expression of several oxidative stress-related biomarkers. Furthermore, CdTe-QD treatment led to apoptosis in the liver via both intrinsic and extrinsic apoptotic pathways. Effects on mitochondria were evidenced by the enlargement and increase in the number of mitochondria in hepatocytes of treated mice. CdTe-QDs also caused changes in the levels and gene expression of electron transport chain enzymes, depletion of ATP, and an increase in the level of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), a regulator of mitochondrial biogenesis. The findings from this study suggest that CdTe-QDs-induced hepatotoxicity might have originated from mitochondrial effects which resulted in oxidative stress and apoptosis in the liver cells. This study provides insight into the biological effects of CdT-QDs at the tissue level and the detailed mechanisms of their toxicity in animals. The study also provides important data for bridging the gap between in vitro and in vivo testing and risk assessment of these NPs.

The bioaccumulation potential and toxic effects of engineered nanomaterials (ENMs) to earthworms are poorly understood. Two studies were conducted following OECD TG 222 on Eisenia fetida to assess the effects of CdTe QDs with different coatings and soil ageing respectively. Earthworms were exposed to carboxylate (COOH), ammonium (NH 4 + ), or polyethylene glycol (PEG) coated CdTe QDs, or a micron scale (bulk) CdTe material, at nominal concentrations of 50, 500 and 2000 mg CdTe QD kg -1 dry weight (dw) for 28 days in Lufa 2.2 soil. In the fresh soil study, earthworms accumulated similar amounts of Cd and Te in the CdTe-bulk exposures, while the accumulation of Cd was higher than Te during the exposures to CdTe QDs. However, neither the total Cd, nor Te concentrations in the earthworms, were easily explained by the extractable metal fractions in the soil or particle dissolution. There were no effects on survival, but some retardation of growth was observed at the higher doses. Inhibition of Na + / K + -ATPase activity with disturbances to tissue electrolytes, as well as tissue Cu and Mn were observed, but without depletion of total glutathione in the fresh soil experiment. Additionally, juvenile production was the most sensitive endpoint, with estimated nominal EC 50 of values >2000, 108, 65, 96 mg CdTe kg -1 for bulk, PEG-, COOH- and NH 4 + -coated CdTe QDs, respectively. In the aged soil study, the accumulation of Cd and Te was higher than in the fresh soil study in all CdTe QD exposures. Survival of the adult worms was reduced in the top CdTe-COOH and -NH 4 + QD exposures by 55 ± 5 and 60 ± 25%, respectively; and with decreases in growth. The nominal EC 50 values for juvenile production in the aged soil were 165, 88, 78 and 63 mg CdTe kg -1 for bulk, PEG-, COOH- and NH 4 + -coated CdTe QDs, respectively. In conclusion, exposure to nanoscale CdTe QDs, regardless of coating, caused more severe toxic effects that the CdTe bulk material and the toxicity increased after soil ageing. There were some coating-mediated effects, likely due to differences in the metal content and behaviour of the materials., Competing Interests: Declaration of competing interest The authors alone are responsible for the content and writing of the paper. The authors report no conflicts of interest., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

The potential toxicity of cadmium-containing quantum dots (QDs) has received much attention because of increasing biomedical applications. However, little has been known about how cadmium telluride (CdTe) QDs influence the gut microbiota and lipid metabolism. In this study, mice were exposed orally to CdTe QDs (200 μL of 0.2, 2, 20 or 200 μm; twice per week) for 4 weeks. The oral experiments showed CdTe QD exposure led to a decrease of the Firmicutes/Bacteroidetes (F/B) ratio of gut microbiota, which highly negatively correlated with the low-density lipoprotein (LDL), triglyceride (TG) and total cholesterol (TC) levels in serum. In addition, the low-dose (0.2 and 2 μm) CdTe QDs significantly increased the diversity of gut microbiota, and did not elevate the LDL, TG and TC levels in serum. The medium dose (20 μm) of CdTe QDs caused the biggest decrease of the F/B ratio, so it significantly increased the LDL, TG and TC levels compared with the control. Furthermore, high-dose (200 μm) CdTe QDs caused various toxicities in the histopathology of liver and intestine, liver function and intestinal immunity, but did not significantly lead to changes of the LDL, TG and TC levels in serum. This study demonstrates that high-dose oral CdTe QDs mainly lead to tissue damage of the liver and intestine, while the medium and low doses of oral CdTe QDs induce shifts of gut microbiota structure, which are associated with blood lipid levels., (© 2020 John Wiley & Sons, Ltd.)

Cadmium-quantum dots (Cd-QDs) possess unique properties as optoelectronic devices for sensitive detection in food and biomedicine fields. However, the toxic effects of Cd-QDs to single cells is still controversial, due to the release mechanism of QDs to Cd 2+ in situ and the cytotoxic effects of QDs and Cd 2+ respectively are still unclear. In this paper, the release rule of Cd 2+ from CdTe QDs within single cells was investigated in situ by using flow cytometry method and the dose-response relationships were explored. Besides, an all-inclusive microscopy system was optimized for live cell imaging to observe the real-time entry process of CdTe QDs into cells. We found that intracellular CdTe QDs and Cd 2+ contents were increased based on the dosage and exposing time. A dissociated saturation of Cd 2+ from CdTe QDs was exist within cells. CdTe QDs induced more serious cytotoxicity on kidney cells than hepatocytes. The toxicity of oxidative stress, cell apoptosis effects induced by CdTe QDs and Cd 2+ are also in consistent with this result. This research develops analytical method to quantify the uptake and release of Cd-QDs to primary cells in situ and can provide technical support in studying the cytotoxicity portion contributed by nanoparticles (NPs) and metal ions., Competing Interests: Declaration of competing interest There are no conflicts to declare., (Copyright © 2020 Elsevier Inc. All rights reserved.)

CdTe quantum dots (QDs) are still widely considered as excellent fluorescent probes because of their far more superior optical performance and fluorescence efficiency than non‑cadmium QDs. Thus, it is important to find ways to control their toxicity. In this study, CdTe QDs and CdTe@ZnS QDs both could cause IL-1ß-mediated inflammation following with pyroptosis in BV2 cells, but the toxic effects caused by CdTe@ZnS QDs was weaker than CdTe QDs, which demonstrated the partial protection of ZnS shell. When investigating the molecular mechanisms of QDs causing the inflammatory injury, the findings suggested that cadmium-containing QDs exposure activated NF-κB that participated in the NLRP3 inflammasome priming and pro-IL-1ß expression. After that, QDs-induced excessive ROS generation triggered the NLRP3 inflammasome activation and resulted in active caspase-1 to process pro-IL-1ß into mature IL-1ß release and inflammatory cell death, i.e. pyroptosis. Fortunately, the inhibitions of caspase-1, NF-κB and ROS or knocking down of NLRP3 all effectively attenuated the increases in the IL-1ß secretion and cell death caused by QDs in BV2 cells. This study provided two methods to alleviate the toxicity of cadmium-containing QDs, in which one is to encapsulate bare-core QDs with a shell and the other is to inhibit their toxic pathways. Since the latter way is more effective than the former one, it is significant to evaluate QDs through a mechanism-based risk assessment to identify controllable toxic targets., Competing Interests: Declaration of Competing Interest Authors of this article declare that there are no conflicts of competing financial interest., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

This study assesses the sex-specific effects induced by CdTe QDs, on the marine mussel Mytilus galloprovincialis in comparison to its dissolved counterpart. A 14 days exposure to CdTe QDs and dissolved Cd was conducted (10 μg Cd L -1 ), analysing Cd accumulation, oxidative stress, biotransformation, metallothionein and oxidative damage in the gonads. Both Cd forms caused significant antioxidant alterations, whereby QDs were more pro-oxidant, leading to oxidative damage, being females more affected. Overall, biochemical impairments on gonads of M. galloprovincialis demonstrate that the reproductive toxicity induced by CdTe QDs in mussels are sex-dependent and mediated by oxidative stress and lipid peroxidation. It is crucial to acknowledge how gametes are affected by metal-based nanoparticles, such as Cd-based QDs. As well as understanding the potential changes they may undergo at the cellular level during gametogenesis, embryogenesis and larval development potentially leading to serious impacts on population sustainability and ecosystem health., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The excellent optical property and relatively low toxicity of CdTe/ZnS core/shell quantum dots (QDs) make them an advanced fluorescent probe in the application of biomedicines, particularly in neuroscience. Thus, it is important to evaluate the biosafety of CdTe/ZnS QDs on the central nervous system (CNS). Our previous studies have suggested that the high possibility of CdTe/ZnS QDs being transported into the brain across the blood-brain barrier resulted in microglial activation and a shift of glycometabolism, but their underlying mechanism remains unclear. In this study, when mice were injected intravenously with CdTe/ZnS QDs through tail veins, the microglial activation, polarized into both M1 phenotype and M2 phenotype, and the neuronal impairment were observed in the hippocampus. Meanwhile, the increased pro- and anti-inflammatory cytokines released from BV2 microglial cells treated with CdTe/ZnS QDs also indicated that QD exposure was capable of inducing microglial activation in vitro. We further demonstrated that the glycolytic shift from oxidative phosphorylation switching into aerobic glycolysis was required in the microglial activation into M1 phenotype induced by CdTe/ZnS QD treatment, which was mediated through the mTOR signaling pathway. The findings, taken together, provide a mechanistic insight regarding the CdTe/ZnS QDs inducing microglial activation and the role of the glycolytic shift in it., (© 2019 John Wiley & Sons, Ltd.)

A rolling-mediated cascade (RMC) amplification strategy is described for improved visualization of profiling glycans of mucin 1 (MUC 1) on cell surfaces. CdTe quantum dots (QDs) are used as fluorescent labels. The RMC based amplification allows even distinct glycoforms of MUC1 to be visualized on the surface of MCF-7 cell via an amplified Förster resonance energy transfer (FRET) imaging strategy that works at excitation/emission wavelengths of 345/610 nm. This is achieved by utilizing antibody against MUC1 modified with the fluorescent label 7-amino-4-methylcoumarin-3-acetic acid (AMCA) as the energy donor in FRET. The QDs (used to label surface glycans) act as acceptors. N-Azidoacetylgalactosamine-Acetylated (Ac4GalNAz) as a non-natural azido sugar, can be incorporated into the glycans of the cell surface, which can promote further labeling. The method has the advantage of only requiring a small amount of non-natural sugar to be introduced in metabolic glycan labeling since too much of an artificial sugar will interfere with the physiological functions of cells. Graphical abstract Schematic for the DNA rolling-mediated cascade (RMC)-assisted metabolic labeling of cell surface glycans by using CdTe quantum dots as labels and an intramolecular amplified FRET strategy for imaging glycans on a specific glycosylated protein, MUC1.

Quantum dots (QDs) are a unique class of nano-materials that have attractive potentials in biological and biomedical applications, and the concern on their biosafety is concomitantly increasing. The overproduction of reactive oxygen species (ROS) is considered to be one of the reasons that induce the in vitro QDs induced toxic response. However, the exact molecular pathways underlying these effects remain poorly clarified and few studies combine the molecular results with the cellular results to explore the cytotoxic effect of QDs. The aim of the present study was to evaluate the effect of mercaptopropionic acid (MPA) capped CdTe QDs on the structures and functions of two antioxidant enzymes, catalase (CAT) superoxide dismutase (SOD), and then associated with the cytotoxic effects of oxidative stress induced by MPA-CdTe QDs on mouse hepatocytes to define the toxic underlying mechanism. The molecular experiment results showed that the exposure of QDs significantly changed the conformation of CAT and SOD, and leading to the promotion of molecular CAT activity and the inhibition of molecular SOD activity. Meanwhile, the cellular experiment results demonstrated that exposure to QDs changed the activities of CAT and SOD in mouse primary hepatocytes, led to the break of redox balance and resulted in the oxidative stress and cell apoptosis. This study explores the effects of MPA- CdTe QDs to the CAT and SOD molecules and then demonstrates the subsequent QDs toxic effects at a cellular level, revealing their potential risk in biomedical applications., (Copyright © 2019 Elsevier B.V. All rights reserved.)

This study describes synthesis of N‑acetyl‑l‑cysteine-capped CdTe quantum dots (QDs) and investigates their interaction with plasma protein fibrinogen (FIB) and the structural changes of FIB. It is shown that the interaction of QDs with FIB is a spontaneous process and the major driving forces are van der Waals forces and hydrogen bonds. Multi-spectroscopic measurements show that the intrinsic fluorescence of FIB was quenched and secondary and tertiary structures were altered due to the interaction with QDs. In addition, the aggregation state of FIB was altered in the presence of QDs. Furthermore, the formed complexes of FIB with QDs reduced the cytotoxicity of QDs. The coating of FIB on QDs could lower intracellular QDs uptake and therefore result in less released cadmium ions and ROS productions. This study, therefore, might be helpful to the comprehensive understanding of QDs toxicity and provide evidence for assessing the safe application of nanoparticles., (Copyright © 2019. Published by Elsevier B.V.)

The application of quantum dots (QDs) is restricted by the biosafety issue. QDs contribute to the adverse effects of organisms probably because of the ability to induce oxidative stress via changing the activity of antioxidant enzyme, for example, superoxide dismutase (SOD). But the underlying molecular mechanisms still remain unclear. This study investigated the harmful effects of oxidative stress induced by mercaptopropionic acid capped CdTe QDs (MPA-CdTe QDs) on the mouse primary nephrocytes as well as the structure and function of SOD molecule and explored the underlying molecular mechanism. After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity. Further molecular experiments showed that the interacting processes between the MPA-CdTe QDs and SOD were spontaneous which changed the conformation, secondary structure of SOD. The interaction significantly resulted in the tightening of polypeptide chains and the shrinkage of SOD, leading to the inhibition of molecular SOD activity. This study demonstrates the adverse effects of QDs, revealing their potential risk in biomedical applications., (© 2019 John Wiley & Sons, Ltd.)

Two different colors of water-soluble core-shell quantum dots CdTe/CdS (green and orange red) have been synthesized and characterized in this paper. The formation of core-shell quantum dots not only improves the fluorescence quantum yield, but also reduces the biological toxicity of quantum dots, and improves the fluorescence lifetime. Two novel fluorescent bioprobes, CdTe/CdS (λ em  = 545 nm)-5-Fu and Bio-CdTe/CdS (λ em  = 600 nm)-TAM, have been synthesized via the interaction of these two core-shell quantum dots with anticancer drugs (5-Fu) and P-gp inhibitors (TAM), respectively. These two fluorescent probes have been simultaneously used in fluorescence imaging of human breast cancer cells MDA-MB-231/MDR. It can be observed that under the action of P-gp inhibitors distributed on the cell membrane, anticancer drugs can be retained in cancer cells. According to the color of quantum dots on the probe, the visualization results of the action of anticancer drugs and P-gp inhibitors can be obtained. This study shows that to prepare functional bioprobes using core-shell quantum dots CdTe/CdS has great potential in the field of biomedical research such as anticancer drugs., (Copyright © 2019. Published by Elsevier B.V.)

Nanotechnology has achieved more commercial attention over recent years, and its application has increased concerns about its discharge in the environment. In this study, we have chosen human hepatic carcinoma (HuH-7) cells because liver tissue has played an important role in human metabolism. Therefore, the objective of this study was to determine DNA damaging and apoptotic potential of cadmium telluride quantum dots (CdTe QDs; average particle size (APS) 10 nm, 1-25 µg/ml) on HuH-7 cells and the basic molecular mechanism of its cellular toxicity. Cytotoxicity of different concentrations of CdTe QDs on HuH-7 cells was determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) and lactate dehydrogenase (LDH) tests. Moreover, reactive oxygen species (ROS) generation, mitochondrial membrane potential, DNA damage, and Hoechst 33342 fluorescent staining morphological analysis of necrotic/apoptotic cells were detected; cellular impairment in mitochondria and DNA was confirmed by JC-1 and comet assay, respectively. A dose- and time-dependent cytotoxicity effect of CdTe QDs exposure was observed HuH-7 cells; the significant ( p < 0.05) cytotoxicity was found at 25 μg/ml of CdTe QDs exposure. The percentage of cytotoxicity of CdTe QDs (25 μg/ml) in HuH-7 cells reached 62% in 48 h. CdTe QDs elicited intracellular ROS generation and mitochondrial depolarization, and DNA integrity cells collectively advocated the apoptotic cell death at higher concentration. DNA damage was observed in cells due to CdTe QDs exposure, which was mediated by oxidative stress. This study exploring the effects of CdTe QDs in HuH-7 cells has provided valuable insights into the mechanism of toxicity induced by CdTe QDs.

Cadmium (Cd)-based QDs are well studied owing to their excellent optical properties. The applications of Cd-based QDs in biomedical filed, however, is hindered by its inherent toxicity. In this study, to overcome the inherent toxicity of heavy metals, CdTe QDs were encapsulated with different shells (NAC, MPA and GSH) to reduce the leakage of Cd from the core. We studied the cytotoxicity of the three kinds of CdTe QDs on S. cerevisiae by spectroscopic, electrochemical, microscopic methods and microcalorimetric technique. Results showed that toxicity of CdTe QDs increased with the augment of QD concentration. According to the values of IC 50 ((GSH-CdTe QDs (15.3 nmol/L) < MPA-CdTe QDs (56.2 nmol/L) < NAC-CdTe QDs (89.8 nmol/L)), the most toxic one is GSH-CdTe QDs, followed by MPA-CdTe QDs, then NAC-CdTe QDs. The coatings have contribution to their toxicity. The three kinds of QDs with the similar shape (sphere) can enter the cell by the clathrin-mediated endocytosis and lead to the different impairments. The mechanism of cytotoxicity is due to the release of Cd 2+ leading elevation of intracellular reactive oxygen species (ROS), which damage mitochondria. The clathrin-mediated endocytosis is a significant factor in determining the toxicity of CdTe QDs., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Quantum dots (QDs), considered as a type of excellent semiconductor nanomaterial, are widely employed and have a number of important applications. However, QDs have the potential to produce adverse effects and toxicity with the underlying molecular mechanisms not well understood. Herein, Caenorhabditis elegans was used for in vivo toxicity assessment to detect the reproductive toxicity of CdTe QDs. We found that exposure to CdTe QDs particles (≥ 50 mg/L) resulted in a defect in reproductive capacity, dysfunctional proliferation and differentiation, as well as an imbalance in oogenesis by reducing the number of cells in pachytene and diakinesis. Further, we identified a SPO-11 and PCH-2 mediated toxic mechanism and a GLP-1/Notch mediated protective mechanism in response to CdTe QDs particles (≥ 50 mg/L). Taken together, these results demonstrate the potential adverse impact of CdTe QDs (≥ 50 mg/L) exposure on oogenesis and provide valuable data and guidelines for evaluation of QD biocompatibility., (Copyright © 2019 Elsevier Inc. All rights reserved.)

In this work, a quick, facile and efficient approach was presented for green synthesis of cadmium telluride quantum dots (CdTe QDs) based on an aqueous extract of the Ficus johannis plant. Two extraction methods involving microwave assisted extraction (MWAE; 90 and 270 w; 15 min) and ultrasonic assisted extraction (USAE; 15 min; 45 °C) were performed as eco-friendly, effective, green and fast techniques for the extract preparation of the fruit's plant. The as-prepared plant extracts were used as natural stabilizing precursors in the synthesis of CdTe QDs. The synthesized QDs were characterized using various techniques. The average particle size of the QDs from the X-ray diffraction patterns was calculated to be 1.2 nm. UV-Vis absorption and fluorescence spectroscopic studies show a wide absorption band from 400 to 425 nm and a maximum emission peak around 470 nm, which confirmed the successful synthesis of CdTe QDs via the applied synthetic method. After synthesis and characterization of the samples, the antimicrobial properties, genotoxicity, toxicity and antifungal activities of the as-prepared CdTe QDs were investigated. In addition, antioxidant properties of the samples (QDs and extracts), were evaluated by different antioxidant assays. The results indicate the significant antimicrobial activity of the extract and CdTe QDs samples, with negligible toxicity and genotoxicity impacts., (Copyright © 2019 Elsevier B.V. All rights reserved.)

In this study, the cytotoxicity of CdTe quantum dots (QDs) of various dimensions was examined using the electroporation method. The influence of the size of QDs on normal and tumour cell viability after 24 h of incubation with nanomaterials was examined. The three human cell lines were chosen for the tests: A549 (a tumour cell line derived from the lung), MRC-5 (normal fibroblasts from the lung) and HaCaT (normal keratinocytes from the skin). Accordingly, we modelled the effect of nanocrystals on various human tissues because nanoparticles can be introduced into an organism through different routes. We were also able to study which cells are more sensitive to nanoparticles: normal or tumour cells. The nanoparticles were introduced into cells through pores in the cell membranes that were generated by electrical pulses. The effectiveness of introducing nanocrystals into cells was determined as a function of the nanocrystal dimensions and accumulation locations. Moreover, the cytotoxicity of quantum dots was tested, and cell viability after electroporation was evaluated. We also investigated whether the introduced nanocrystals released cadmium ions., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Microglial cells are resident immune cells in the central nervous system. Activation of microglia as induced by CdTe quantum dots (QDs) can trigger damage to neurons. To quantify the intracellular QDs, we monitored the intracellular Cd concentration in the QD-exposed mouse microglial cells (BV-2 cell line). The extent of cell injury at different times correlated with the Cd concentration in cells at that time. In addition to Cd ion detection, we also monitored the intracellular fluorescence of the QDs. More QDs accumulated in the nucleus than in the cytoplasm. Comet assays confirmed that QDs induce DNA damage. However, DNA cannot interact with QDs, so the DNA damage was not caused by CdTe QDs adducts to DNA but by the increase of the Cd ion concentration and the secondary oxidative damage. In addition to DNA damage, biofilm injury and endogenous reduced glutathione depletion were also apparent in QD-exposed BV-2 cells. These changes can be prevented or even reversed by exogenous reduced glutathione administration., (© 2018 John Wiley & Sons, Ltd.)

Fluorescent CdTe nanocrystals (NCs) capped with beta-cyclodextrin (β-CD) are successfully synthesized by host-guest supramolecular assembly of the hydrophobic alkyl chains of N-acetyl-l-cysteine (NAC) on the surface of CdTe NCs and eco-friendly β-CD via the promising simple hydrothermal method in our experiments. The as-prepared NCs display better stability and lower toxicity compared with traditional those only capped with NAC. Specially, cytotoxicity experiments to human umbilical vein endothelial cells in vitro and zebrafish embryo toxicological tests in vivo are performed to determine the toxicity of CdTe NCs. For their practical applications, the promising red-luminescent NCs are employed as stable and low poison red phosphors to fabricate white light-emitting diodes (WLEDs) with remarkable color-rendering index (CRI) being 91.6. This research offers significance for solving the difficulty in toxicity and instability of heavy metal based NCs, which has potential applications in future optoelectronic devices and biomarkers., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Adenosine triphosphate-binding cassette (ABC) transporters, including P-glycoprotein (Pgp) and multi-resistance associated proteins (Mrps), have been considered important participants in the self-protection of zebrafish embryos against environmental pollutants, but their possible involvement in the efflux and detoxification of quantum dots (QDs), as well as their regulation mechanism are currently unclear. In this work, gene expression alterations of ABC transporters, nuclear receptors, and oxidative stress signaling in zebrafish embryos after the treatment of mercaptopropionic acid (MPA)CdTe QDs and MPA-CdSCdTe QDs were investigated. It was observed that both QDs caused concentration-dependent delayed hatching effects and the subsequent induction of transporters like mrp1&2 in zebrafish embryos, indicating the protective role of corresponding proteins against CdTe QDs. Accompanying these alterations, expressions of nuclear receptors including the pregnane X receptor (pxr), aryl hydrocarbon receptor (ahr) 1b, and peroxisome proliferator-activated receptor (ppar)-β were induced by QDs in a concentration- and time-dependent manner. Moreover, elevated oxidative stress, reflected by the reduction of glutathione (GSH) level and superoxide dismutase (SOD) activities, as well as the dramatic induction of nuclear factor E2 related factor (nrf) 2, was also found. More importantly, alterations of pxr and nrf2 were more pronounced than that of mrps, and these receptors exhibited an excellent correlation with delayed hatching rate in the same embryos (R 2  > 0.8). Results from this analysis demonstrated that the induction of mrp1 and mrp2 could be important components for the detoxification of QDs in zebrafish embryos. These transporters could be modulated by nuclear receptors and oxidative stress signaling. In addition, up-regulation of pxr and nrf2 could be developed as toxic biomarkers of CdTe QDs., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The authors evaluated the cytotoxicity underlying mechanisms of biogenic tellurium (Te) nanorods (NRs) produced by the Pseudomonas pseudoalcaligenes strain Te on the PC12 cell line. The half-maximal inhibitory concentration (IC 50 ) value was estimated at 5.05 ± 0.07 ng/ml for biogenic Te NRs and 2.44 ± 0.38 ng/ml for K 2 TeO 3 , respectively. The viability of PC12 was inhibited concentration dependent at doses of 1, 2.5, 5, 10, and 20 ng/ml. Te NRs principally induced late apoptosis or necrosis at IC 50 concentration, without effect on caspase-3 activities. Furthermore, Te NRs reduced glutathione and enhanced malondialdehyde levels, and also reduced superoxide dismutase and catalase activities. These findings revealed that biogenic Te NRs were less toxic than K 2 TeO 3 . Additionally, they induced cytotoxity towards the PC12 cell line through the activation of late apoptosis independent of the caspase pathway, and may also enhance oxidative stress in the nervous system.

There are now over a thousand nano-containing products on the market and the antibacterial properties of some nanomaterials has created interest in their use as cleaning agents, biocides and disinfectants. Engineered nanomaterials (ENMs) are being released into the environment and this raises concerns about their effects on microbes in the receiving ecosystems. This study evaluated the bacterial toxicity of a wide range of nanomaterials with different surface coatings on Escherichia coli K-12 MG1655. The minimum inhibitory concentration (MIC) assay, which quantifies the threshold for growth inhibition in suspensions of bacteria, was used to rank the toxicity of silver (Ag), cupric oxide (CuO), cadmium telluride (CdTe) quantum dots, titanium dioxide (TiO 2 ), nanodiamonds and multi-walled carbon nanotubes (MWCNTs). Bacteria were exposed for 12 h at 37 °C to a dilution series of the test suspensions in 96-well plates. The precision and accuracy of the method was good with coefficients of variation < 10%. In terms of the measured MIC values, the toxicity order of the ENMs was as follows: CdTe quantum dots ammonium-coated, 6 mg L -1 > Ag nanoparticles, 12 mg L -1 > CdTe quantum dots carboxylate-coated, 25 mg L -1 > CdTe quantum dots polyethylene glycol-coated, 100 mg L -1 . The MIC values were above the highest test concentration used (100 mg L -1 ) for CuO, TiO 2 , nanodiamonds and MWCNTs, indicating low toxicity. The MIC assay can be a useful tool for the initial steps of ENMs hazard assessment., (Copyright © 2018 Elsevier Inc. All rights reserved.)