The present study consisted of cytotoxic, genotoxic, and oxidative stress responses of human neuroblastoma cell line (IMR32) following exposure to different doses of cerium oxide nanoparticles (CeO2 NPs; nanoceria) and its microparticles (MPs) for 24 hours. Cytotoxicity was evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays whereas genotoxicity was assessed using the cytokinesis-block micronucleus and comet assays. A battery of assays including lipid peroxidation, reactive oxygen species (ROS), hydrogen peroxide, reduced glutathione, nitric oxide, glutathione reductase, glutathione peroxidase, superoxide dismutase, catalase, and glutathione S-transferase were performed to test the hypothesis that ROS was responsible for the toxicity of nanoceria. The results showed that nanosized CeO2 was more toxic than cerium oxide MPs. Hence, further study on safety evaluation of CeO2 NPs on other models is recommended.

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Nanoparticles (NPs) apart from their widespread advantages and increased utilisation, have aroused concerns over their safe use. Nickel (II) oxides (NiO) NPs are used as catalysts, biosensors and in many of the consumer products. The increasing use of NiO NPs necessitates an improved understanding of their potential impact on the environment and human health. In this study, we investigated the acute genotoxic effects of NiO NPs by oral route administration with three different doses (125, 250 and 500 mg/kg bw). Before the in vivo toxicological evaluation, characterisation of particles by Transmission Electron Microscopy, X-ray diffraction, Dynamic Light Scattering (DLS) and Laser Doppler Velocimetry analysis was performed. Genotoxicity biomarkers such as comet, micronucleus and chromosomal aberrations (CAs) assays were utilised in this study. To document the uptake, retention and elimination of the NPs, biodistribution studies were also performed. The particle size obtained from Transmission Electron Microscopy analysis for NiO NPs was 15.62 ± 2.59 nm. The mean hydrodynamic diameter and PdI of NiO NPs in Milli-Q water suspension obtained by DLS was 168.9 ± 17.13 nm and 0.375, respectively. Comet assay revealed significant (P < 0.001) DNA damage at 500 mg/kg bw dose in the PBL, liver and kidney cells of rats at the 24-h sampling time. The result of micronucleus and CAs tests was in agreement with the comet assay data. Biodistribution of NiO NPs revealed a maximum accumulation of Ni in the liver tissue at the 24-h sampling time. Our study showed significant DNA damage at the high dose level and the effect was more prominent at 24-h sampling time, providing preliminary evidence that the NiO NPs are capable of inducing genotoxicity when administered through the oral route. However, mechanistic investigations are needed before drawing any firm conclusion regarding the toxicology of NiO NPs.

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A series of novel ethyl 2,7-dimethyl-4-oxo-3-[(1-phenyl-1H-1,2,3-triazol-4-yl)methyl]-4,5-dihydro-3H-pyrano[2,3-d]pyrimidine-6-carboxylate derivatives 7a - 7m were efficiently synthesized employing click chemistry approach and evaluated for in vitro cytotoxic activity against four tumor cell lines: A549 (human lung adenocarcinoma cell line), HepG2 (human hematoma), MCF-7 (human breast adenocarcinoma), and SKOV3 (human ovarian carcinoma cell line). Among the compounds tested, the compounds 7a, 7b, 7f, 7l, and 7m have shown potential and selective activity against human lung adenocarcinoma cell line (A549) with IC ranging from 0.69 to 6.74 μm. Molecular docking studies revealed that the compounds 7a, 7b, 7f, 7l, and 7m are potent inhibitors of human DNA topoisomerase-II and also showed compliance with stranded parameters of drug likeness. The calculated binding constants, k , from UV/VIS absorptional binding studies of 7a and 7l with CT-DNA were 10.77 × 10 , 6.48 × 10 , respectively. Viscosity measurements revealed that the binding could be surface binding mainly due to groove binding. DNA cleavage study showed that 7a and 7l have the potential to cleave pBR322 plasmid DNA without any external agents.

The exigency of semiconductor and super capacitor tungsten oxide nanoparticles (WO NPs) is increasing in various sectors. However, limited information on their toxicity and biological interactions are available. Hence, we explored the underlying mechanisms of toxicity induced by WO NPs and their microparticles (MPs) using different concentrations (0-300 μg ml ) in human lung carcinoma (A549) cells. The mean size of WO NPs and MPs by transmission electron microscopy was 53.84 nm and 3.88 μm, respectively. WO NPs induced reduction in cell viability, membrane damage and the degree of induction was size- and dose-dependent. There was a significant increase in the percentage tail DNA and micronuclei formation at 200 and 300 μg ml after 24 hours of exposure. The DNA damage induced by WO NPs could be attributed to increased oxidative stress and inflammation through reactive oxygen species generation, which correlated with the depletion of reduced glutathione content, catalase and an increase in malondialdehyde levels. Cellular uptake studies unveiled that both the particles were attached/surrounded to the cell membrane according to their size. In addition, NP inhibited the progression of the cell cycle in the G /M phase. Other studies such as caspase-9 and -3 and Annexin-V-fluorescein isothiocyanate revealed that NPs induced intrinsic apoptotic cell death at 200 and 300 μg ml concentrations. However, in comparison to NPs, WO MPs did not incite any toxic effects at the tested concentrations. Under these experimental conditions, the no-observed-significant-effect level of WO NPs was determined to be ≤200 μg ml in A549 cells.

The genotoxicological effects in 200 lead acid storage battery recycling and manufacturing industry workers in Hyderabad along with matched 200 controls were studied. The genetic damage was determined by comet, micronucleus (MN), and chromosomal aberration (CA) test in peripheral blood lymphocytes (PBL). The MN test was also carried out in buccal epithelial cells (BECs). Pb in ambient air, blood Pb (B-Pb) concentrations, and hematological parameters were measured. The superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and malondialdehyde (MDA) formed were also studied. The results of the present study showed that there was a statistically significant (P < 0.01) increase in mean percent tail DNA, frequency of CA, and MN in PBL as well as in BEC as compared to controls. Pb in ambient air and B-Pb concentrations were found to be significantly higher (P < 0.01). The hematocrit, hemoglobin, and red blood cell values were significantly lowered in Pb-exposed workers in comparison to controls. SOD, GPx, and CAT levels were significantly decreased while GSH and MDA levels increased in exposed group when compared to control group. The present study suggests that environmental health standards should be enforced to control Pb contamination from battery industries to reduce human health risk.

The outcome of the study revealed an increased risk of genotoxicity and health implications in female agricultural workers.