Nanoplastics (NPs) are particles ranging in size between 1 and 1000 nm, and they are a form of environmental contaminant of great ecotoxicological concern. Although NPs are widespread across ecosystems, they have only recently garnered growing attention from both the scientific community and regulatory bodies. The present study reviews scientific literature related to the exposure and effects of NPs and identifies research gaps that impede the finalization of related environmental risk assessments (ERAs). Approximately 80 articles published between 2012 and 2021 were considered. Very few studies (eight articles) focused on the presence of NPs in biotic matrices, whereas the majority of the studies (62 articles) assessed the lethal and sublethal effects of NPs on aquatic and terrestrial organisms. Whilst many studies focused on nude NPs, only a few considered their association with different aggregates. Amongst NPs, the effects of polystyrene are the most extensively reported to date. Moreover, the effects of NPs on aquatic organisms are better characterized than those on terrestrial organisms. NP concentrations detected in water were close to or even higher than the sublethal levels for organisms. An ERA framework specifically tailored to NPs is proposed.

Cadmium is classified as a human carcinogen, and its disturbance in zinc homeostasis has been well established. However, its extent as well as molecular mechanisms involved in cadmium carcinogenesis has yet to be fully clarified. To this end, we used the zinc specific probe Zinquin to visualize and to quantitatively evaluate changes in the concentration of labile zinc, in anin vitromodel of human hepatic cells (HepG2) exposed to cadmium. A very large increase (+93%) of intracellular labile zinc, displaced by cadmium from the zinc proteome, was measured when HepG2 were exposed to 10 µM cadmium for 24 hrs. Microarray expression profiling showed that in cells, featuring an increase of labile zinc after cadmium exposure, one of the top regulated genes isSnail1(+3.6), which is included in the adherens junction pathway and linked to cancer. In the same pathwayMET,TGF-βR, and two members of the Rho-family GTPase,Rac, andcdc42all implicated in the loss of adherence features and acquisition of migratory and cancer properties were regulated, as well. The microRNAs analysis showed a downregulation of miR-34a and miR-200a, both implicated in the epithelial-mesenchymal transition. These microRNAs results support the role played by zinc in affecting gene expression at the posttranscriptional level.

Cadmium and cadmium compounds are contaminants of the environment, food, and drinking water and are important constituents of cigarette smoke. Cd exposure has also been associated with airborne particulate CdO and with Cd-containing quantum dots in medical therapy. Adverse cadmium effects reported in the literature have stimulated during recent years an ongoing discussion to better elucidate cadmium outcomes at cell and molecular level. The present work is designed to gain an insight into the mechanism of p53 impairment at gene and protein level to understand Cd-induced resistance to apoptosis. We used a hepatoma cell line (HepG2) derived from liver, known to be metal responsive. At genotoxic cadmium concentrations no cell cycle arrest was observed. The p53 at gene and protein level was not regulated. Fluorescence images showed that p53 was correctly translocated into the nucleus but that thep21Cip1/WAF-1, a downstream protein of p53 network involved in cell cycle regulation, was not activated at the highest cadmium concentrations used. The miRNAs analysis revealed an upregulation of mir-372, an miRNA able to affectp21Cip1/WAF-1expression and promote cell cycle progression and proliferation. The role of metallothioneins and possible conformational changes of p53 are discussed.