The effect of polystyrene nanoplastics on arsenic-induced apoptosis in HepG2 cells.

Microplastics are detrimental to the environment. However, the combined effects of microplastics and arsenic (As) remain unclear. In this study, we investigated the combined effects of polystyrene (PS) microplastics and As on HepG2 cells. The results showed that PS microplastics 20, 50, 200, and 500 nm in size were taken up by HepG2 cells, causing a decrease in cellular mitochondrial membrane potential. The results of lactate dehydrogenase release and flow cytometry showed that PS microplastics, especially those of 50 nm, enhanced As-induced apoptosis. In addition, transcriptome analysis revealed that TP53, AKT1, CASP3, ACTB, BCL2L1, CASP8, XIAP, MCL1, NFKBIA, and CASP7 were the top 10 hub genes for PS that enhanced the role of As in HepG2 cell apoptosis. Our results suggest that nano-PS enhances As-induced apoptosis. Furthermore, this study is important for a better understanding of the role of microplastics in As-induced hepatotoxicity.

Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics.

Microplastics (MPs) are widespread in the environment and can be ingested through food, water, and air, posing a threat to human health. In addition, MPs can have a potential combined effect with other toxic compounds. Polystyrene (PS) has been shown to enhance the cytotoxicity of okadaic acid (OA). However, it remains unclear whether this enhancement effect is related to the size of PS particles. In this study, we investigated the mechanism of the combined effect of PS microplastics (PS-MPs) or PS nanoplastics (PS-NPs) and OA on Caco-2 cells. The results indicated that PS-NPs enhanced the cytotoxicity of OA and induced endoplasmic reticulum (ER) stress-mediated apoptosis in Caco-2 cells, compared to PS-MPs. Specifically, PS-NPs and OA cause more severe oxidative stress, lactate dehydrogenase (LDH) release, and mitochondrial membrane depolarization. Furthermore, it induced intracellular calcium overload through store-operated channels (SOCs) and activated the PERK/ATF-4/CHOP pathway to cause ER stress. ER stress promoted mitochondrial damage and finally activated the caspase family to induce apoptosis. This study provided an indirect basis for the assessment of the combined toxicity of MPs or NPs with OA.

Differences in toxicity induced by the various polymer types of nanoplastics on HepG2 cells.

The problem of microplastics (MPs) contamination in food has gradually come to the fore. MPs can be transmitted through the food chain and accumulate within various organisms, ultimately posing a threat to human health. The concentration of nanoplastics (NPs) exposed to humans may be higher than that of MPs. For the first time, we studied the differences in toxicity, and potential toxic effects of different polymer types of NPs, namely, polyethylene terephthalate (PET), polyvinyl chloride (PVC), and polystyrene (PS) on HepG2 cells. In this study, PET-NPs, PVC-NPs, and PS-NPs, which had similar particle size, surface charge, and shape, were prepared using nanoprecipitation and emulsion polymerization. The results of the CCK-8 assay showed that the PET-NPs and PVC-NPs induced a decrease in cell viability in a concentration-dependent manner, and their lowest concentrations causing significant cytotoxicity were 100 and 150 µg/mL, respectively. Moreover, the major cytotoxic effects of PET-NPs and PVC-NPs at high concentrations may be to induce an increase in intracellular ROS, which in turn induces cellular damage and other toxic effects. Notably, our study suggested that PET-NPs and PVC-NPs may induce apoptosis in HepG2 cells through the mitochondrial apoptotic pathway. However, no relevant cytotoxicity, oxidative damage, and apoptotic toxic effects were detected in HepG2 cells with exposure to PS-NPs. Furthermore, the analysis of transcriptomics data suggested that PET-NPs and PVC-NPs could significantly inhibit the expression of DNA repair-related genes in the p53 signaling pathway. Compared to PS-NPs, the expression levels of lipid metabolism-related genes were down-regulated to a greater extent by PET-NPs and PVC-NPs. In conclusion, PET-NPs and PVC-NPs were able to induce higher cytotoxic effects than PS-NPs, in which the density and chemical structure of NPs of different polymer types may be the key factors causing the differences in toxicity.

Exosomal miRNA analysis provides new insights into exposure to nanoplastics and okadaic acid.

As an emerging environmental pollutant, nanoplastics (NPs) have attracted wide attention in terms of their impact on the ecological environment and human health. Currently, researches on the cytotoxicity of NPs mainly focus on oxidative stress, damage to the cell membrane and organelles, induction of immune response and genotoxicity. Okadaic acid (OA) is the main component of diarrheal shellfish toxin. Based on the previous combined toxicity exploration of polystyrene (PS) NPs and (OA) to human gastric adenocarcinoma (AGS) cells, cell-derived exosomes were extracted and exosomal miRNA profiles were analyzed for the first time in this study. The results showed that the composition of miRNAs varied after the exposure of NPs and OA. Specifically, the expression of miR-1-3p in both PS-Exo and PS-OA-Exo was significantly reduced. And the expression of miR-1248 was upregulated most significantly by comparing the DE miRNAs between PS-Exo and PS-OA-Exo. MiR-1-3p and miR-1248 may be the key genes for the combined toxicity of NPs and OA. After analysis, we found that both the decreased expression of miR-1-3p and the increased expression of miR-1248 can increase the expression of FN1 and affect DNA replication, which was surprisingly consistent with the results of our previous cytotoxicity studies. Since exosomal miRNAs are selectively encapsulated by donor cell, we speculate that the changes of exosomal miRNAs may due to the synchronous changes of intracellular environment and the downregulation of intracellular FN1 may be attributed to decreased expression of miR-1-3p and increased expression of miR-1248 in donor cells. Accordingly, we come to the conclusion that the changes of miRNAs in the exosomes derived from AGS cells after environmental stimulation could reflect the biological effects of donor cells.

Polydopamine molecularly imprinted polymer coated on a biomimetic iron-based metal-organic framework for highly selective fluorescence detection of metronidazole.

Molecular imprinting technology was used to coat polydopamine (PDA) onto MIL-53(Fe) surface by simple self-polymerization. The MIL-53(Fe)@MIP composite with enhanced peroxidase-like activity and specific target recognition function was synthesized and selected to construct a fluorescence sensor to detect metronidazole (MNZ). Since the substrate terephthalic acid was incorporated in the framework of MIL-53(Fe)@MIP, no additional luminescent substrate was required. This avoided the interference of the substrate on the enzymatic detection system and improved the accuracy of the assay. The characteristics of MIL-53(Fe)@MIP composite were investigated and confirmed by systematic analyses. The experimental results proved that the sensor provided satisfactory performances for quantitative determination of MNZ in wide linear range from 1 to 200 µM with low limit of detection as 53.4 nM. Potential interfering substances such as common cations and anions, amino acids, other antibiotics, sugars, and food additive were studied to show negligible effect on the assay, allowing the practical application to different fields including milk and human serum by the standard addition method. The recoveries were obtained between 93.2 and 102%, and the RSD was less than 3%.

Ultrasensitive turn-on fluorescent detection of trace thiocyanate based on fluorescence resonance energy transfer.

Thiocyanate (SCN(-)) is a small anion byproduct of cyanide metabolism. Several methods have been reported to measure SCN(-) above the micromolar level. However, SCN(-) is derived from many sources such as cigarettes, waste water, food and even car exhaust and its effect is cumulative, which makes it necessary to develop methods for the detection of trace SCN(-). In this paper, a simple and ultrasensitive turn-on fluorescence assay of trace SCN(-) is established based on the fluorescence resonance energy transfer (FRET) between gold nanoparticles (AuNPs) and fluorescein. The detection limit is 0.09 nM, to the best of our knowledge, which has been the lowest detection LOD ever without the aid of costly instrumentation. The fluorescence of fluorescein is significantly quenched when it is attached to the surface of AuNPs. Upon the addition of SCN(-), the fluorescence is turned on due to the competition action between SCN(-) and fluorescein towards the surface of AuNPs. Under an optimum pH, AuNPs size and concentration, incubation time, the fluorescence enhancement efficiency [(IF-I0)/I0] displays a linear relationship with the concentration of SCN(-) in the range of 1.0 nM to 40.0 nM. The fluorescein-AuNP sensor shows absolutely high selectivity toward SCN(-) than other 16 anions. The common metal ions, amino acids and sugars have no obvious interference effects. The accuracy and precision were evaluated based on the recovery experiments. The cost effective sensing system is successfully applied for the determination of SCN(-) in milk products and saliva samples.