This work reports on the toxicity of CuO nanoparticles (NPs) to maize (Zea mays L.) and their transport and redistribution in the plant. CuO NPs (100 mg L(-1)) had no effect on germination, but inhibited the growth of maize seedlings; in comparison the dissolved Cu(2+) ions and CuO bulk particles had no obvious effect on maize growth. CuO NPs were present in xylem sap as examined by transmission electron microscopy (TEM) and energy dispersive spectroscopy (EDS), showing that CuO NPs were transported from roots to shoots via xylem. Split-root experiments and high-resolution TEM observation further showed that CuO NPs could translocate from shoots back to roots via phloem. During this translocation, CuO NPs could be reduced from Cu (II) to Cu (I). To our knowledge, this is the first report of root-shoot-root redistribution of CuO NPs within maize. The current study provides direct evidence for the bioaccumulation and biotransformation of CuO NPs (20-40 nm) in maize, which has significant implications on the potential risk of NPs and food safety.

Graphene-family nanomaterials (GFNs) including pristine graphene, reduced graphene oxide (rGO) and graphene oxide (GO) offer great application potential, leading to the possibility of their release into aquatic environments. Upon exposure, graphene/rGO and GO exhibit different adsorption properties toward environmental adsorbates, thus the molecular interactions at the GFN-water interface are discussed. After solute adsorption, the dispersion/aggregation behaviors of GFNs can be altered by solution chemistry, as well as by the presence of colloidal particles and biocolloids. GO has different dispersion performance from pristine graphene and rGO, which is further demonstrated from surface properties. Upon exposure in aquatic environments, GFNs have adverse impacts on aquatic organisms (e.g., bacteria, algae, plants, invertebrates, and fish). The mechanisms of GFNs toxicity at the cellular level are reviewed and the remaining unclear points on toxic mechanisms such as membrane damage are presented. Moreover, we highlight the transformation routes of GO to rGO. The degradation of GFNs upon exposure to UV irradiation and/or biota is also reviewed. In view of the unanswered questions, future research should include comprehensive characterization of GFNs, new approaches for explaining GFNs aggregation, environmental behaviors of metastable GO, and the relationship between dispersion of GFNs and the related adsorption properties.

Novel physicochemistries of engineered nanomaterials (ENMs) offer considerable commercial potential for new products and processes, but also the possibility of unforeseen and negative consequences upon ENM release into the environment. Investigations of ENM ecotoxicity have revealed that the unique properties of ENMs and a lack of appropriate test methods can lead to results that are inaccurate or not reproducible. The occurrence of spurious results or misinterpretations of results from ENM toxicity tests that are unique to investigations of ENMs (as opposed to traditional toxicants) have been reported, but have not yet been systemically reviewed. Our objective in this manuscript is to highlight artifacts and misinterpretations that can occur at each step of ecotoxicity testing: procurement or synthesis of the ENMs and assessment of potential toxic impurities such as metals or endotoxins, ENM storage, dispersion of the ENMs in the test medium, direct interference with assay reagents and unacknowledged indirect effects such as nutrient depletion during the assay, and assessment of the ENM biodistribution in organisms. We recommend thorough characterization of initial ENMs including measurement of impurities, implementation of steps to minimize changes to the ENMs during storage, inclusion of a set of experimental controls (e.g., to assess impacts of nutrient depletion, ENM specific effects, impurities in ENM formulation, desorbed surface coatings, the dispersion process, and direct interference of ENM with toxicity assays), and use of orthogonal measurement methods when available to assess ENMs fate and distribution in organisms.

The toxicity of CuO nanoparticles (NPs) to human lung epithelial (A549) cells was investigated in this study. CuO NPs (10-100 mg/L) had significant toxicity to A549 cells, whereas CuO bulk particles (BPs) showed much lower toxicity (24 h IC(50), 58 and 15 mg/L for CuO BPs and NPs, respectively). Transmission electron microscopic analysis demonstrated CuO NP entry into A549 cells and organelles, including lysosomes, mitochondria, and nucleus. Endocytosis was the primary pathway of CuO NPs uptake. CuO NPs (15 mg/L) induced mitochondrial depolarization, possibly mediated by reactive oxygen species (ROS) generation. Intracellular CuO NPs first generate ROS, which subsequently induces the expression of p38 and p53 and ultimately causes DNA damage (Comet assay). We confirm for the first time that the primary cytotoxic response is oxidative stress rather than DNA damage. A fraction of the CuO NPs was exported to the extracellular environment. In this study, centrifugal ultrafiltration tubes were successfully employed to determine the dissolved Cu(2+) from CuO NPs in the cell medium. Dissolved Cu(2+) ions contributed less than half of the total toxicity caused by CuO NPs, including ROS generation and DNA damage. This study provided useful data for understanding transport and toxicity of metal oxide NPs in human cells.

This is the first study investigating the toxicity of nanoparticles (NPs) to algae in the presence of dissolved organic matter (DOM). Suwannee river fulvic acid (SRFA), a type of DOM, could significantly increase the toxicity of CuO NPs to prokaryotic alga Microcystis aeruginosa. Internalization of CuO NPs was observed for the first time in the intact algal cells using high resolution transmission electron microscopy (HRTEM), and the cell uptake was enhanced by SRFA. A fast Fourier transformation (FFT)/inversed FFT (IFFT) process revealed that a main form of intracellular NPs was Cu(2)O, and an intracellular environment may reduce CuO into Cu(2)O. The internalization behavior alone did not seem to pose a hazard to membrane integrity as shown from the flow cytometry data. Elevated CuO nanotoxicity by SRFA was related to a combination of a lesser degree of aggregation, higher Cu(2+) release, and enhanced internalization of CuO NPs.

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The key roles of NOM affecting environmental processes and toxicity of MNPs in aquatic environments are discussed and presented.

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