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Micro- and nanoplastics (MNPLs) are intentionally produced for commercial uses (primary MNPLs) or are formed from environmentally aged plastics (secondary MNPLs). Independent of their origin, all of them will finally end up in the environment constituting some of the known emergent pollutants. Despite the inert nature of plastics, questions about their potential biological effects on human health need to find sound answers. In addition, the association between the potentially induced effects and the MNPL size is also required to be known. In this context, we have used our in vivomodel of Drosophilalarvae and three nanopolystyrene plastics (PSNPLs) sized 50, 200, and 500 nm (PS-50, PS-200, and PS-500) to add new data to better understand the potential health risks of MNPLs. Our model has permitted us to visualize (viatransmission electron microscopy, TEM) the journey of the PSNPLs administered viaingestion, their interaction with gut lumen components (including symbiotic microbiota), their uptake by gut enterocytes, their translocation through the intestinal barrier to the hemolymph, and their uptake by hemocytes. This behavior was observed for the three analyzed sizes and, for the largest sizes, changes in size/shape were observed in ingested PSNPLs. Although no relevant toxicity, as measured by the egg-to-adult viability, was observed, exposure induced a wide molecular response altering the expression of genes involved in the general stress response, in the antioxidant response and even in the genotoxicity response, as well as in genes related to the intestinal damage response. Furthermore, a general induction of ROS production and DNA damage was also detected. Interestingly, these types of responses were size-dependent with the small PSNPL size inducing a higher response.

Accumulation of plastic and its derivatives, micro- and nanoplastics (MNPLs), is a substantial environmental and ecological problem that could potentially become a serious health concern to humans. In this study, we propose an attractive approach to obtain new data, using polystyrene nanoparticles (PSNPs) as a model, to understand the risk of human exposure to MNLPs. Whole blood samples from different donors were exposed ex vivoto different concentrations of PSNPs for 24, 48, or 72 h. The effects were analyzed in different subsets of white peripheral blood cells (WBCs), namely lymphocytes, monocytes, and polymorphonuclear (PMN) cells, to assess specific cellular sensitivity. Our results showed no significant toxicity of PSNPs when evaluated in the overall WBC population. Nevertheless, different lineages manifested sharp differences between cell types with very limited uptake in lymphocytes, very high uptake in monocytes, and with intermediate uptake values for PMN cells. Furthermore, a significant increase in the levels of DNA damage was observed in monocytes and PMN cells after PSNP exposure, but not in lymphocytes. Interestingly, our results showed that PSNP exposure induced changes in the whole blood secretome. These findings were further confirmed when the expression of different cytokines was analyzed, revealing a significant increase in the expression of different cytokines related to the inflammatory, immune, and stress response, as well as cell proliferation.

The ubiquitous and increasing presence of micro-/nanoplastics (MNPLs) in our environment demands an urgent hazard assessment, in order to determine the potential risk they pose to human beings. Given the scarce information found in the literature regarding MNPL's effects over human cells, the aim of our work is to evaluate MNPL's ability to penetrate the cells, and their potential toxic/genotoxic effects. To this aim, we used polystyrene MNPLs, as they are a widespread model of synthetic polymer, using nanoparticles with (y-nPS) or without (nPS) a fluorescent label. The human colon adenocarcinoma Caco-2 cell line was used as the cellular target, as ingestion is one of the main entry routes of MNPLs. Different endpoints were analyzed as indicators of nanotoxicity, including cytotoxicity, ROS increase, genotoxicity, DNA oxidative damage and increase in the expression of stress-related genes.

Nanomaterials in general and cobalt nanoparticles (CoNPs) in particular are of great interest not only because of their multiple applications and environmental impact, but also for their potential toxicity and safety issues. Since most of the mechanisms involved in the toxicity of CoNPs are not very well known, mainly in vivo, we used Drosophila melanogasteras a simple and reliable in vivomodel to investigate some toxicity-involved mechanisms. Thus, several toxicity-related approaches are used in this study including physicochemical characterization, viability, internalization, intracellular oxidative stress, and DNA damage (comet assay). In addition, changes in the expression of genes involved in general stress and antioxidant response, as well as in DNA repair response were evaluated, to better understand the underlying molecular mechanisms. The effects of CoNPs were compared with those induced by cobalt chloride (CoCl2), as a model ion releasing agent, to determine the role of the nanosized shapes in the observed responses. The obtained results indicate that ingested CoNPs translocate through the intestinal barrier of Drosophilalarvae affecting hemolymph cells. Hemocytes, as targeted cells, show higher levels of intracellular reactive oxygen species (ROS) after CoCl2exposure, but lower levels of DNA damage, in comparison with those induced by CoNPs. In addition, different genes showed an altered expression pattern, accordingly, if larvae were exposed to CoCl2or to CoNPs. Subsequently, the effects induced by CoNPs cannot be associated only with their chemical nature.