Combined toxicity of QD-Cu~(2+) on L02 cells and protective effect of NAC
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The oxidative injury of individual QDs or Cu2+ to hepatic cells were both reported,the combined toxicity is concerned due to the co-existence of these two chemicals in human liver.We thus employed human hepatic L02 cells to test the combined toxicity of QDs and Cu2+(lower toxicity) through the cell viability decrease and cell morphology changes,meanwhile,the protective effect of antioxidant reagent NAC was used to evaluate the oxidant injury associated toxicity mechanism.The results showed that both QDs and Cu2+ could decrease the cells viability,and addition of IC10 of QDs could significantly improve Cu2+ induced cell toxicity with cell viability decrease up to 300 %.NAC showed remarkable protective effects with almost identical cell viability and cell morphology compared to the control,indicating the coexistence of lower toxicity of QDs could improve Cu2+ induced L02 cells toxicity,and NAC could effectively decrease QDs-Cu2 induced oxidant injury toxicity.Keywords:
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Scientific information on the potential harmful effects of silver nanoparticles (AgNPs) on human health severely lags behind their exponentially growing applications in consumer products. In assessing the toxic risk of AgNP usage, liver, as a detoxifying organ, is particularly important. The aim of this study was to explore the toxicity mechanisms of nano and ionic forms of silver on human hepatoblastoma (HepG2) cells. The results showed that silver ions and citrate-coated AgNPs reduced cell viability in a dose-dependent manner. The IC50 values of silver ions and citrate-coated AgNPs were 0.5 and 50 mg L−1, respectively. The LDH leakage and inhibition of albumin synthesis, along with decreased ALT activity, indicated that treatment with either AgNP or Ag ions resulted in membrane damage and reduced the cell function of human liver cells. Evaluation of oxidative stress markers demonstrating depletion of GSH, increased ROS production, and increased SOD activity, indicated that oxidative stress might contribute to the toxicity effects of nano and ionic forms of silver. The observed toxic effect of AgNP on HepG2 cells was substantially weaker than that caused by ionic silver, while the uptake of nano and ionic forms of silver by HepG2 cells was nearly the same. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 679–692, 2016.
Silver nanoparticle
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Copper toxicity
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Objective This study aimed to the evaluate the nephrotoxicity of CdSe/ZnS QDs in vitro and vivo, as well as investigate the underlying toxicity mechanisms. Results In vitro experiments showed that compared with control cells, CdSe/ZnS QDs treatment significantly inhibited cell viability and promoted cell apoptosis in dose-dependent manner in NRK cells. Notably, CdSe/ZnS QDs treatment increased the contents of MDA and ROS, and decreased the activities of SOD, CAT and GSH-Px; however, the co-treatment of NAC and QDs relieved the oxidative damage of NRK cells. Moreover, in vivo experiments also revealed that CdSe/ZnS QDs treatment obviously increased kidney weight coefficient, damaged the kidney function, as well as induced inflammatory response and inhibited the activation of NRF2/Keap1 pathway in kidney tissues of mice. Conclusions CdSe/ZnS QDs exhibited obvious nephrotoxicity by mediating oxidative damage and inflammatory response in vitro and in vivo via NRF2/Keap1 pathway. Methods The characterization of CdSe/ZnS QDs was analyzed by transmission electron microscope, emission spectrum scanning, and dynamic light scattering. Rat kidney cells (NRK) were exposed to different doses of CdSe/ZnS QDs with or without N-acetylcysteine (NAC, antioxidant). Then, cellular uptake of CdSe/ZnS QDs was detected, and in vitro cytotoxicity was evaluated by MTT assay and TUNEL assay.
Nephrotoxicity
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Abstract There has been rapid growth in nanotechnology in both the public and private sectors worldwide, but concern about nanosafety exists. To assess size-dependent cytotoxicity on human cancer cells, we studied the cytotoxic effect of three kinds of zinc oxide nanoparticles (ZnO NPs) on human epithelial colorectal adenocarcinoma (Caco-2) cells. Nanoparticles were first characterized by size, distribution, and intensity. Multiple assays have been adopted to measure the cell activity and oxidative stress. The cytotoxicity of ZnO NPs was time dependent and dose dependent. The 24-h exposure was chosen to confirm the viability and accessibility of the cells and taken as the appropriate time for the following test system. The IC 50 value was found at a low concentration. The oxidative stress elicited a significant reduction in glutathione with increase in reactive oxygen species and lactate dehydrogenase. The toxicity resulted in a deletion of cells in the G1 phase and an accumulation of cells in the S and G2/M phases. One type of metallic oxide (ZnO) exerted different cytotoxic effects according to different particle sizes. Data from the previous experiments showed that 26-nm ZnO NPs appeared to have the highest toxicity to Caco-2 cells. The study demonstrated the toxicity of ZnO NPs to Caco-2 cells and the impact of particle size, which could be useful in the medical applications.
Nanochemistry
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To explore the potential biological activities of transition metal-based nanoparticles (NPs), we synthesized two copper-based NPs, CuI and Cu3(PO4)2. The structural features of these NPs were determined by the X-ray diffraction (XRD), dynamic light scattering (DLS) and transmission electron microscopy (TEM). The size of CuI and Cu3(PO4)2 NPs were 35 ± 4.2 nm and 67 ± 6.3 nm respectively as determined by TEM. Cell viability, generation of reactive oxygen species (ROS), cell cycle and induction of apoptosis were assessed on human breast cancer cell line MCF7 after the treatment of these NPs. Exposure of CuI and Cu3(PO4)2 NPs decreased cell viability in a dose-dependent manner. Also, CuI NPs produced more ROS compared to Cu3(PO4)2 and presence of N-acetyl cysteine (NAC) along with NPs increased the cell survival. Cell cycle analysis indicated that after exposure of these NPs at their respective LD50 doses increased Sub G1 and G2/M peak after 8 h and 24 h of treatment respectively. Apoptosis study by AnnexinV-FITC staining showed slight increased in the early and late apoptosis after 8 h of treatment and most of the cells were dead after 24 h of treatment. Thus our observations suggest that the exposure of these two NPs induced dose-dependent cytotoxicity on MCF7 cell that is associated with ROS-mediated apoptosis.
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Recent evidence suggests that some nanomaterials, which are widely used in many fields, have health effects. In order to investigate the cytotoxicity induced by nanosized copper particles (nano-Cu), PC12 cells, which were widely used as an in vitro model for the neuron research, were treated with different concentrations (0, 1, 10, 30, and 100 lg/mL) of nano-Cu. The cell viability was determined by mea- surement of the reduction product of 3-(4,5-dimethyl- thiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT). The oxidative stress induced by nano-Cu and its possible mechanism were studied in relation to the generation of reactive oxygen species (ROS) and the cellular activity of superoxide dismutase (SOD). Results showed that incubation of PC12 cells with increasing concentrations of nano-Cu induced a decrease of cell viability in a concentration- and time- dependent manner. In addition, flow cytometry assay using Annexin V-FITC/PI staining was used to inves- tigate the mode of nano-Cu-induced cell death and quantified the percentage of apoptotic cells. Results showed that nano-Cu induced the significant apoptosis in PC12 cells. Meanwhile, intracellular accumulation of ROS was increased with the increased concentrations of nano-Cu and it was associated with decreased SOD activity, which was probably due to protect effects against the oxidative stress in PC12 cells. Results suggested that both excessive intracellular ROS and decreased SOD contributed to nano-Cu-induced cyto- toxicity. In other words, the increasing of oxidative stress was a key mechanism in PC12 apoptosis induced by nano-Cu.
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The objective of this study was to examine the cytotoxic effects of binary mixtures of Al2O3 and ZnO NPs using mouse fibroblast cells (L929) and human bronchial epithelial cells (BEAS-2B) as biological test systems. The synergistic, additive, or antagonistic behavior of the binary mixture was also investigated. In toxicity experiments, cellular morphology, mitochondrial function (MTT assay), apoptosis, nuclear size and shape, clonogenic assays, and damage based upon oxidative stress parameters were assessed under control and NPs exposure conditions. Although Abbott modeling results provided no clear evidence of the binary mixture of Al2O3 and ZnO NPs exhibiting synergistic toxicity, some specific assays such as apoptosis, nuclear size and shape, clonogenic assay, activities of antioxidant enzymatic enzymes catalase, superoxide dismutase, and levels of glutathione resulted in enhanced toxicity for the mixtures with 1 and 1.75 toxic units (TU) toward both cell types. Data demonstrated that co-presence of Al2O3 and ZnO NPs in the same environment might lead to more realistic environmental conditions. Our findings indicate cytotoxicity of binary mixtures of Al2O3 and ZnO NPs produced greater effects compared to toxicity of either individual compound.
Clonogenic assay
Nanotoxicology
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With the widespread use of quantum dots (QDs), the likelihood of exposure to quantum dots has increased substantially. The application of quantum dots in numerous biomedical areas requires detailed studies on their toxicity. In this study, we aimed to determine the threshold dose which reduced or eliminated CdTe-induced toxicity in L929 cells by controlling the exposure dose. We established a cellular model of acute exposure to CdTe QDs. Cells were exposed to different concentrations of CdTe QDs (2.2 nm and 3.5 nm) followed by illustrative cytotoxicity analysis. The results showed that low concentrations of CdTe QDs (under 10 µg/mL) promoted cell viability, caused no obvious effect on the rate of cell apoptosis, intracellular calcium levels and changes in mitochondrial membrane potential, while high concentrations significantly inhibited cell viability. In addition, reactive oxygen species in the 10 µg/mL-treated group was significantly reduced compared with the control group. In summary, the cytotoxicity of CdTe QDs on L929 cell is dose-dependent, time-dependent and size-dependent. Low concentrations of CdTe QDs (below 10 µg/mL) may be nontoxic and safe in L929 cells, whereas high concentrations (above 10 µg/mL) may be toxic resulting in inhibition of proliferation and induction of apoptosis in L929 cells.
Viability assay
Cadmium telluride photovoltaics
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Cadmium sulfide quantum dots(CdS QDs)were synthesized using emulsion liquid membrane system. The cytotoxicity and mechanism of CdS QDs to cells were studied. Human fetal liver cells(L-02)were selected as models. L-02 cells were exposed to CdS QDs with different concentrations(0.00, 1.25, 2.50, 5.00, 10.00, 20.00 and 40.00μg·mL-1) for 24h, then the content of GSH and the activity of LDH and SOD were determined; Moreover, the influence of addition of N-Acetylcysteine(NAC) on the viability of cells was compared; The concentration cadmium ion both inside and outside cells were detected. Results showed that, compared with the control group, the viability of cells exposed to CdS QDs significantly decreased(p0.05 or p0.01). In CdS QDs-NAC joint exposure groups, the viability of cells increased significantly(p0.01)in groups of 10.00, 20.00 and 40.00μg·mL-1. The extracellular Cd2+ concentration was higher than the intracellular Cd2+ concentration, except the 5.00μg·mL-1 group which the intracellular Cd2+ concentration is slightly higher than the extracellular Cd2+ concentration. Cellular LDH increased gradually with the increase of CdS QDs concentrations. Compared with the control group, both SOD activity in 40.00μg·mL-1 group and GSH contents in 20.00μg·mL-1 group decreased significantly(p0.05). Cd2+ can permeate the cell membrane easily and then into the cells, resulting in cell damage. Oxidative damage may be the mechanism of CdS QDs cytotoxicity.
Cadmium sulfide
Viability assay
Cadmium chloride
Fetal bovine serum
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