With the widespread occurrence and accumulation of plastic waste in the world, plastic pollution has become a serious threat to ecosystem and ecological security, especially to estuarine and coastal areas. Understanding the impacts of changing nanoplastics concentrations on aquatic organisms living in these areas is essential for revealing the ecological effects caused by plastic pollution. In the present study, we revealed the effects of exposure to gradient concentrations (0.005, 0.05, 0.5 and 50 mg/L) of 75 nm polystyrene nanoplastics (PS-NPs) for 48 h on metabolic processes in muscle tissue of a bivalve, the razor clam Sinonovacula constricta, via metabolomic and transcriptomic analysis. Our results showed that PS-NPs caused dose-dependent adverse effects on energy reserves, membrane lipid metabolism, purine metabolism and lysosomal hydrolases. Exposure to PS-NPs reduced energy reserves, especially lipids. Membrane lipid metabolism was sensitive to PS-NPs with contents of phosphocholines (PC), phosphatidylethanolamines (PE) and phosphatidylserines (PS) increasing and degradation being inhibited in all concentrations. High concentrations of PS-NPs altered the purine metabolism via increasing contents of guanosine triphosphate (GTP) and adenine, which may be needed for DNA repair, and consuming inosine and hypoxanthine. During exposure to low concentrations of PS-NPs, lysosomal hydrolases in S. constricta, especially cathepsins, were inhibited while this influence was improved transitorily in 5 mg/L of PS-NPs. These adverse effects together impacted energy metabolism in S. constricta and disturbed energy homeostasis, which was manifested by the low levels of acetyl-CoA in high concentrations of PS-NPs. Overall, our results revealed the effects of acute exposure to gradient concentrations of PS-NPs on S. constricta, especially its metabolic process, and provide perspectives for understanding the toxicity of dynamic plastic pollution to coastal organisms and ecosystem.

The contamination of the aquatic environment by plastic nanoparticles is becoming a major concern due to their potential adverse effects in aquatic biota. Therefore, in-depth knowledge of their uptake, trafficking and effects at cellular and systemic levels is essential to understand their potential impacts for aquatic species. In this work, zebrafish (Danio rerio) was used as a model and our aims were: i) to determine the distribution, uptake, trafficking, degradation and genotoxicity of polystyrene (PS) NPs of different sizes in a zebrafish cell line; ii) to study PS NPs accumulation, migration of immune cells and genotoxicity in larvae exposed to PS NPs; and iii) to assess how PS NPs condition the survival of zebrafish larvae exposed to a pathogen and/or how they impact the resistance of an immunodeficient zebrafish. Our results revealed that the cellular distribution differed depending on the particle size: the 50 nm PS NPs were more homogeneously distributed in the cytoplasm and the 1 μM PS NPs more agglomerated. The main endocytic mechanisms for the uptake of NPs were dynamin-dependent internalization for the 50 nm NPs and phagocytosis for the 1 μm nanoparticles. In both cases, degradation in lysosomes was the main fate of the PS NPs, which generated alkalinisation and modified cathepsin genes expression. These effects at cellular level agree with the results in vivo, since lysosomal alkalization increases oxidative stress and vice versa. Nanoparticles mainly accumulated in the gut, where they triggered reactive oxygen species, decreased expression of the antioxidant gene catalase and induced migration of immune cells. Finally, although PS NPs did not induce mortality in wild-type larvae, immunodeficient and infected larvae had decreased survival upon exposure to PS NPs. This fact could be explained by the mechanical disruption and/or the oxidative damage caused by these NPs that increase their susceptibility to pathogens.

Epidemiological studies have demonstrated that the general population’s exposure to bisphenol A (BPA) substitutes is ubiquitous. Bisphenol F (BPF), one of the main BPA substitutes, is increasingly replacing BPA in plastics for food and beverage applications. Accumulating evidence suggests that BPA exposure is associated with nonalcoholic fatty liver disease (NAFLD)-like changes. However, the potential effects of BPF on lipid homeostasis remain poorly understood. In the present study, an epidemiological analysis with LC-MS-MS revealed that the BPF concentrations in the serum of NAFLD patients were significantly higher than those in a control group. Supporting this result, using Oil Red O, BODIPY 493/503, LipidTox Deep Red staining and gas chromatography-time-of-flight mass spectrometry (TOF-MS) assays, we found that BPF exposure induced NAFLD-like changes, with obvious lipid droplet deposition, triglyceride (TG) and fatty acids increase in mouse livers. Meanwhile, lipid droplet deposition and TG increase induced by BPF were also observed in HepG2 cells, accompanied by autophagic flux blockade, including autophagosome accumulation and the decreased degradation of SQSTM1/p62. Using adenoviruses dual-reporter plasmid RFP-GFP-LC3, RFP-GFP-PLIN2 transfection, AO staining, and EGFR degradation assays, we demonstrated that BPF treatment impaired lysosomal degradative capacity, since BPF treatment obviously impaired lysosomal acidification, manifested as decreased lysosomal hydrolase cathepsin L (CTSL) and mature cathepsin D (CTSD) in HepG2 and mouse liver issues. Additionally, v-ATPase D, a multi-subunit enzyme that mediates acidification of eukaryotic intracellular organelles, significantly decreased after BPF exposure in both the vitro and in vivo studies.This study ascertained a novel mechanism involving dysfunctional of lysosomal degradative capacity induced by BPF, which contributes to lipophagic disorders and causes lipid droplet deposition. This work provides evidence that lysosomes may be a target organelle where BPF exerts its potential toxicity; therefore, novel intervention strategies targeting lysosome are promising for BPF-induced NAFLD-like changes.