Table 2.
QD | Model | Administration | QD concentration | Exposure duration | Toxicity | Ref |
---|---|---|---|---|---|---|
CdS-QDs | Soybean plants | Growth medium | 50–200 mg/L | 14 days | Peroxidases play the predominant role in quenching the oxidative stress caused by CdS-QD exposure. At the highest CdS-QD treatment (200 mg/L), root lignification allowed the plants to restrict Cd accumulation, except in QD-PVP, where lignification was reduced by 21% leading to higher Cd content in shoots | Majumdar et al. 2019 |
CdSe and CdSe/ZnS | Escherichia coli (E. coli, represents a prokaryotic system) and Phanerochaete chrysosporium (P. chrysosporium, represents eukaryotic system) | In vitro and growth medium | 0, 10, 20, 50, and 80 nM | 48 h | Bioaccumulation amounts of CdSe QDs by E. coli and P. chrysosporium were larger than those of CdSe/ZnS QDs due to the smaller particle size and less negative surface charges of CdSe QDs. | Hu et al. 2019 |
CdSe QD, CdSe/ZnS QD | Shewanella oneidensis MR-1 | In vitro | A total volume of 150 μL at varying concentrations | 15 min | QD interaction leads to membrane disruption, which is mechanical and depends on the QD concentration and their affinity to the liposome membranes | Williams et al. 2018 |
CdSe/ ZnS | SPF grade female and male BABL/c mice | Subcutaneous injection | 5.0, 1.0, and 0.1 pmol/day/mouse | 14 days | QDs are found in the ovaries, but no changes are detected on the behavior and estrous cycle on the female mice. The mRNA downregulations of FSHr and LHr are observed, and the number of matured oocytes had shown a significant decrease when the QDs dosage was above 1.0 pmol/day along with a decrease in fertilization rate | Xu et al. 2016 |
CdSe/ZnS | Human hepatic cell line L02 and 8-week-old male C57BL/6 mice |
In vitro (L02), IV injection (mice) |
20, 40, and 80 nM (L02) 10 nmol/kg body weight (mice) |
48 h (L02) 2 weeks (mice) |
CdSe/ZnS QDs conjugated with carboxyl groups induced hepatocyte pyroptosis, and liver inflammation and dysfunction. The in vitro and in vivo hepatic toxicity of QDs was mediated by QDs-induced NLRP3 activation which was attributed to Ca2+ mobilization and mtROS production after exposure to QDs | Lu et al. 2016 |
CdSe/ZnS | TK6, BEAS-2B, and HFF-1 | In vitro | 0–20 nM | 24 h | Cytotoxicity and genotoxicity are strongly affected by a multitude of parameters including (1) differences in cell type potentially resulting in varying surface area contact with the exposed material, in addition to inherent cellular differences in internalizing NPs and ability to cope with an exogenous insult; (2) the nature of the QD surface chemistry; (3) the degree of QD agglomeration in the presence of varying amounts of serum proteins; (4) differences in cell culture media composition; and (5) time of exposure | Lin et al. 2015 |
CdSe@MSA and CdSe(S)@MSA QDs | Escherichia coli | In vitro | 0–4000 nM | 100 min | The toxicity observed for CdSe QDs may be directly linked to •OH radicals produced | Kauffer et al. 2014 |
TGA/TGH-CdTe | HeLa cells and Kunming mice | In vitro, intravenous injection (in vivo) |
In vitro: 45 mg m/L In vivo: 0.4 (low dose), 2.0 (representing medium dose) and 10.0 (representing high dose) mg kg1 |
24 h | PEG modification played an important role in reducing the toxicity of the QDs. PEG conjugated with the QD surface through chemical bonds and thus altered their surface state. Furthermore, PEG formed a fence-like structure on the QD surface, which could more effectively prevent Cd2+ release, which was induced by the diffusion effect from the QD surface to the solution | Du et al. 2019 |
GSH-CdQDs and MPA-CdQDs | Lemna minor | Direct exposure | 0–15 mg/L | 168 h | GSH- and MPA-capped Cd-based QDs have similar toxicity for L. minor but are significantly less toxic than CdCl2 | Modlitbová et al. 2018 |
CdS QDs | Yeast strains | Transcriptomic analysis | 0.25 mg/L | 24 h | In this case, yeast can be a good model to correlate genes with human orthologues in a cross-species comparison that might help to elucidate the response to toxic insults, like to CdS QDs, at a system level as well as to predict the mode of action of similar compounds in other species | Pasquali et al. 2017 |
Negatively charged: MPA-CdTe/ZnS QDs, MPA/MPO-CdTe/ZnS QDs, NAC-CdTe/ZnS QDs, GSH-CdTe/ZnS QDs |
E. coli | Optical density (OD) assays | 2 h | QDs decrease the growth rate of E. coli. The inhibition ratio of positive QDs is higher than that of negative QDs | Lai et al. 2017 | |
Positively charged: CA-CdTe QDs and CA-CdTe/ZnS QDs | ||||||
CdTe | Liver mitochondria from female Wistar rats | Direct exposure | 100 nM | 60 min | Two kinds of QDs, coated with MPA and TGA respectively, could impair mitochondrial energy metabolism and affect mitochondrial lipid peroxidation | Xiang et al. 2017 |
CdTe | Male BALB/c mice | IV injection | High dose of 2.0 nmol per mouse and a low dose of 0.2 nmol per mouse | 90 days | Bodyweight measurements demonstrated there was no overt toxicity for both dose at day 90 after exposure, but the high dose CdTe affected body weight up to 15 days after exposure | Lin et al. 2015 |
CdTe | 8-week-old male mice | Intravenous administration | 4.125, 8.25, and 16.5 mg/kg | 4 weeks | Increased the level of lipid peroxides marker, MDA, in the liver | Zhang et al. 2015a, b |
CdTe and CdTe@ZnS QDs | Caenorhabditis elegans | Foraging behavior assay | 0.001, 0.01, 0.1, and 1 g/L (CdTe) 0.1 and 1 g/L (CdTe@ZnS QDs) | Neurotoxicity of CdTe QDs at concentrations of 0.1–1 g/L on both the development and function of RMEs motor neurons in nematodes. Data demonstrate the impairment of foraging behavior after CdTe QDs exposure and imply the possible severe ecological risk of long-term exposure to low concentrations of CdTe QDs to environmental animals | Zhang et al. 2015a, b | |
CdTe | Bombyx mori | IV injection | 0.08 nM and 0.32 nM | 48 h | Time and dose-dependent damage in the hematopoietic organ and hematocytes. With ROS might be one of the influencing mechanisms | Liu et al. 2014 |
CdS | Mytilus galloprovincialis | In vitro | 0.001, 0.01, 0.1, 1, 10, 25, 50, and 100 mg Cd/L | 24 h | CdS QDs exposures decreased the cell viability of both hemocytes and gill cells. Main mechanisms of toxicity of CdS QDs in mussel hemocytes and gill cells involve ROS production and genotoxicity | Katsumiti et al. 2014 |
Phospholipid micelle encapsulated CdSe/CdS/ZnS QDs | Kunming mice | IV injection | 0.81 mg (7.2 μmol)/kg | 14 days | QD exposure with a short buffering period before conception does not cause overt pregnancy complications or significant toxicity effects | Xiang et al. 2017 |