Titanium dioxide nanoparticles (TiO₂NPs) are increasingly used in consumer products, industrial and medical applications, raising concerns on their potential toxicity. The available in vitro and in vivo studies on these NPs show controversial results. Crystalline structure is the physicochemical characteristic that seems to influence mainly TiO₂NPs toxicity, so its effect needs to be further studied. We aimed to study whether and how crystalline form influences potential cyto-genotoxic and inflammatory effects induced by two commercial TiO₂NPs (TiO₂-A, mainly anatase; TiO₂-B, mainly rutile) in human alveolar A549 and bronchial BEAS-2B cells exposed to 1–40 µg/mL. Cell viability (WST-1), membrane damage (LDH release), IL-6, IL-8 and TNF-α release (ELISA) and direct/oxidative DNA damage (fpg-comet assay) were evaluated. Physicochemical characterization included analysis of crystalline form (TEM and XRD), specific surface area (BET), agglomeration (DLS) and Z-potential (ELS). Our results show that TiO₂-A NPs induce in BEAS-2B cytotoxicity and a slight inflammation and in A549 slight oxidative effects, whereas TiO₂-B NPs induce genotoxic/oxidative effects in both cell lines, revealing different toxicity mechanisms for the two tested NPs. In conclusion, our study confirms the influence of crystalline form on cellular response, also demonstrating the suitability of our in vitro model to screen early TiO₂NPs effects.

This study aimed to identify sensitive and noninvasive biomarkers of early cyto-genotoxic, oxidative and inflammatory effects for exposure to volatile organic compounds (VOCs) in shipyard painters. On 17 (11 spray and 6 roller) painters (previously characterized for VOCs exposure to toluene, xylenes, ethylbenzene, ethyl acetate) and on 18 controls, we performed buccal micronucleus cytome (BMCyt) assay; Fpg-comet assay on lymphocytes; detection of urinary 8-oxoGua (8-oxo-7,8-dihydroguanine), 8-oxodGuo (8-oxo-7,8-dihydro-2′-deoxyguanosine) and 8-oxoGuo (8-oxo-7,8-dihydroguanosine), and cytokines release on serum. We found induction of cyto-genotoxicity by BMCyt assay and inflammatory effects (IL-6 and TNFα) in roller painters exposed to lower VOC concentrations than spray painters. In contrast, in both worker groups, we found direct and oxidative DNA damage by comet assay (with slightly higher oxidative DNA damage in roller) and significant increase of 8-oxoGuo and decrease of 8-oxodGuo and 8-oxoGua in respect to controls. The cyto-genotoxicity observed only on buccal cells of roller painters could be related to the task’s specificity and the different used protective equipment. Although limited by the small number of subjects, the study shows the usefulness of all the used biomarkers in the risk assessment of painters workers exposed to complex mixtures.

Poly(ADP-ribose)polymerase-1 (PARP1) is a nuclear protein implicated in DNA repair, recombination, replication, and chromatin remodeling. The aim of this study was to evaluate possible differences between PARP1^−/− and wild-type mice regarding induction and repair of DNA lesions in irradiated male germ cells. Comet assay was applied to detect DNA damage in testicular cells immediately, and two hours after 4 Gy X-ray irradiation. A similar level of spontaneous and radiation-induced DNA damage was observed in PARP1^−/− and wild-type mice. Conversely, two hours after irradiation, a significant level of residual damage was observed in PARP1^−/− cells only. This finding was particularly evident in round spermatids. To evaluate if PARP1 had also a role in the dynamics of H2AX phosphorylation in round spermatids, in which γ-H2AX foci had been shown to persist after completion of DNA repair, we carried out a parallel analysis of γ-H2AX foci at 0.5, 2, and 48 h after irradiation in wild-type and PARP1^−/− mice. No evidence was obtained of an effect of PARP1 depletion on H2AX phosphorylation induction and removal. Our results suggest that, in round spermatids, under the tested experimental conditions, PARP1 has a role in radiation-induced DNA damage repair rather than in long-term chromatin modifications signaled by phosphorylated H2AX.

Cancer cases have been estimated that will increase in the next years with consequent increase of antineoplastic (AD) drug treatments and workers handling these hazardous chemicals. We aimed to evaluate genotoxic/oxidative effects of AD exposure by fpg-comet assay on a large size sample of workers (214 exposed and 164 controls) involved in preparation; administration, including Hyperthermic intraperitoneal chemotherapy (HIPEC) and pressurized intraperitoneal aerosol chemotherapy (PIPAC); and disposal. With the final aim to identify suitable early biomarkers of genotoxic effect useful to health surveillance, we correlated fpg-comet assay (blood) and Buccal Micronucleus Cytome (BMCyt) assay data. Fpg-comet parameters resulted higher in the exposed group vs. controls, demonstrating direct and oxidative DNA damage in workers handling ADs. Fpg-comet direct DNA damage and genotoxic parameters of BMCyt assay demonstrated a weak statistically significant correlation. This cross-sectional study is one of the few available evaluating both direct and oxidative DNA damage due to ADs on a large sample size of workers and correlating fpg-comet and BMCyt assay results. It highlights the need to evaluate genotoxic effects by both the biomarkers and furnishes a contribution to their validation. Moreover, we demonstrate for the first time oxidative DNA damage on workers performing HIPEC and PIPAC administration.

Graphene and its various derivatives, known as graphene-based nanomaterials (GBNs), hold tremendous potential across many fields due to their exceptional properties. As with any novel material, concerns about their safety have emerged alongside their widespread production and use. Several studies have shown that GBNs can have diverse effects on various cell lines and organisms under different exposure conditions. This study intends to evaluate the potential toxicity of few-layer graphene (FLG) in human bronchial BEAS-2B. Cells were exposed to different concentrations of FLG for 24 h, and the cyto-genotoxic, oxidative, and inflammatory effects were evaluated. We found an increase in cytotoxicity in terms of cell death, cell apoptosis, and membrane damage at the highest concentration. We also detected a slight increase in direct DNA damage and the percentage of comets. Oxidative DNA damage was observed at the highest concentration. FLG exposure did not induce notable cytokine release. Overall, this study suggests that exposure to FLG can induce cytotoxicity, apoptosis, and DNA damage in BEAS-2B, particularly at high concentrations. These findings contribute to a better understanding of the potential health effects of FLG and highlight the importance of considering dose-dependent effects when assessing the safety of GBNs.