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Graphene can be modified by different functional groups through various transformation processes in the environment. The toxicological activity of graphene is closely related to its ability to produce reactive oxygen species (ROS), which can be altered by surface modification. Herein, unfunctionalized graphene (u-G), carboxylated graphene (G-COOH) and aminated graphene (G-NH2) were selected to determine their ability to photogenerate ROS in the aqueous phase. Oxidative stress (ROS concentration and superoxide dismutase activity) in Daphnia magnaunder simulated sunlight radiation induced by the materials was also investigated. Based on density functional theory (DFT) calculations, the photochemical pathways of ROS production were identified. G-COOH and G-NH2produced singlet oxygen in the aqueous phase by mediating energy transfer. G-COOH, G-NH2and u-G generated superoxide anions and further produced hydroxyl radicals by inducing electron transfer. By comparing the biological redox potential and the lowest occupied molecular orbital values (ELUMO) of the substances, u-G and G-COOH were identified to have the potential to induce oxidative stress. The predictive results were validated by the significant increase of oxidative stress biomarkers in Daphnia magna. By coupling experimental observations with the theoretical predictions, the results provide mechanistic insight into understanding the photochemical activity and toxicity of graphene and its surface-functionalized derivatives.

Despite considerable research effort devoted to the study of the effects of silver nanoparticles on mammalian cells in recent years, data on the potential long term effects of this nanomaterial remain scarce, and centered on epithelial cells. The aim of this study was to explore the effects of silver nanoparticles on macrophages. To this end, RAW 264.7 murine macrophages were exposed to either 1 μg ml−1silver nanoparticles for 20 days, i.e.a chronic exposure scheme, or to 20 μg ml−1silver nanoparticles for 24 hours, i.e.an acute exposure scheme. A proteomic study was then conducted to study and compare the cellular responses to both exposure schemes. They proved to be essentially different, and stronger for the chronic exposure scheme. Targeted validation studies showed effects of chronic exposure to silver nanoparticles on detoxifying enzymes such as flavin reductase, which was increased, and on central metabolism enzymes such as triose phosphate isomerase, the activity of which decreased under chronic exposure to silver nanoparticles. Chronic exposure to silver nanoparticles also induced a decrease of reduced glutathione content, a decreased phagocytic activity and reduced macrophage responses to lipopolysaccharide, as exemplified by nitric oxide and interleukin 6 production. Overall, chronic exposure to silver nanoparticles induced stronger effects than acute exposure on macrophages in the metabolic (glutathione level, mitochondrial potential) and functional (phagocytosis, cytokine production) parameters tested.

Silver nanoparticles are known to strongly affect biological systems, and numerous toxicological studies have investigated their effects. Most of these studies examine the effects immediately following acute exposure. In this work, we have conducted further investigation by studying not only the acute, post-exposure response, but also the cellular response after a 72 hour-recovery-phase post exposure. As a biological model we have used macrophages, which are very important cells with respect to their role in the immune response to particulate materials. To investigate the response of macrophages to nanoparticles and their recovery post exposure, we have used a combination of proteomics and targeted experiments. These experiments provided evidence that the cellular reaction to nanoparticles, including the reaction during the recovery phase, is a very active process involving massive energy consumption. Pathways such as the oxidative stress response, central and lipid metabolism, protein production and quality control are strongly modulated during the cellular response to nanoparticles, and restoration of basic cellular homeostasis occurs during the recovery period. However, some specialized macrophage functions, such as lipopolysaccharide-induced cytokine and nitric oxide production, did not return to their basal levels even 72 hours post exposure, showing that some effects of silver nanoparticles persist even after exposure has ceased.

Anatase titanium dioxide nanoparticles (TiO2-NPs) are generally observed to have a higher cellular toxicity than rutile TiO2-NPs, which is mainly ascribed to the increased generated amount of intracellular reactive oxygen species (ROS) and thereby the greater oxidative damage of anatase TiO2-NPs. However, close attachment between nanoparticles (NPs) and cells is a prerequisite for the inducement of intracellular ROS generation. Cell surface bound and soluble exopolymeric substances (B-EPS and S-EPS, respectively) can play an important role in the cell–NPs interaction and regulate the difference in the nanotoxicity of different NPs, which has not been specifically investigated. Interactions of S-EPS and B-EPS extracted from green algae (Chlorella pyrenoidosa) with anatase and rutile TiO2-NPs and the effect of EPS on the algal accumulation and toxicity of the NPs were therefore investigated. Results show that the anatase TiO2-NPs had a significantly higher adsorption of B-EPS than the rutile TiO2-NPs, which could contribute to the greater heteroagglomeration with the algae and the higher algal toxicity of the anatase TiO2-NPs. S-EPS had a higher adsorption on the two NPs than B-EPS; and the adsorption of S-EPS in the bulk solution increased homoaggregation and sedimentation of the NPs, which could inhibit the algal accumulation and toxicity of the NPs. The association with B-EPS greatly increased the apparent algal accumulation of the NPs, but the accumulated NPs could mainly be located on cell surfaces rather than entering the cells, as evidenced by the transmission electron microscopy observation. Thus, B-EPS could act as a bio-barrier protecting the cell wall and membranes from the direct attack of NPs and limiting the cell internalization of NPs. However, the algal cell associated NPs would transfer through food chains with algae, which could cause potential ecological effects and warrants further study. These results will be helpful for assessing the fate and ecological effects of NPs.

Graphene oxide (GO) can affect the antibacterial ability of antibiotics by serving as an antibiotic carrier. However, the mechanisms for the antibacterial activity of a combination of GO and antibiotics are not known. In this study, we examined the effect of GO on the antibacterial activity of three antibiotics (i.e., lincomycin hydrochloride (LMH), chloramphenicol (CPC) and gentamycin sulfate (GMS)) against Gram-negative Escherichia colibacteria (e.g. E. coli) and Gram-positive Staphylococcus aureusbacteria (e.g. S. aureus). GO will coat on the bacteria and cause cell membrane damage, assisting growth inhibition of bacteria, with a stronger effect on S. aureusthan E. coli. The inactivation of E. coliand S. aureuswith bare GO is concentration- and time-dependent. The presence of GO increases or decreases the antibacterial ability of antibiotics, depending on the interaction of GO with the antibiotic, the interaction of GO with bacteria, and the sensitivity of bacteria to the antibiotic. The contact order of GO, the antibiotic and the bacterium has a notable effect on the combined antibacterial activity of antibiotics and GO. The pretreatment of GO with bacteria will increase the antibacterial ability of LMH and CPC significantly, while LMH and CPC show relatively low sensitivity to bacteria. The combination of GO and different antibiotics provides different extents of antibacterial efficiency toward microorganisms.

Copper has been investigated as a promising alternative for SCR reactions. However, most Cu-based catalysts supported on zeolites, alumina or titania produced a certain amount of undesired N2O by-product. Herein, we report a strategy to tune the redox properties of copper oxides viaconfinement within titanate nanotubes (Cu/TNTs) and investigate their SCR activity as well as the N2selectivity. The Cu/TNT catalyst showed an excellent NO reduction performance (above 90%) in the temperature window of 300–450 °C and the N2selectivity could exceed 98% among the whole reaction temperature range of 150–470 °C, with a negligibly low concentration of N2O being detected. After systematic characterizations, the tuning of the chemical state of copper and oxygen, the remarkable adsorption capability, the accelerated oxidation of Cu+to Cu2+, the lower level of NH3oxidation and ultimately the tuning of redox properties were discovered. This work could provide a new approach to design SCR catalysts with superior catalytic reduction performance as well as excellent N2selectivity.