Although there is increasing concern about the toxicity of nanoplastics, the effects of nanoplastic exposure and subsequent recovery on immune responses, as well as antioxidant responses and gut microbiota, in crustaceans are rarely reported. In this study, the nonspecific immunity and antioxidant defense of Eriocheir sinensis were evaluated after acute exposure to various concentrations (0, 2.5, 5, 10 and 20 mg/L) of 75-nm polystyrene nanoplastics (PS-NPs) for 48 h, as well as after 7 days of recovery from the nanoplastic environment. The results showed that, after 48 h of exposure, nanoplastics were observed in the gills, hepatopancreas and gut. However, no nanoplastics were found in the gut after 7 days of recovery. Under nanoplastic-induced stress, Hc, Relish, proPO, and LITAF mRNA levels increased in the gills and hepatopancreas for 48 h. Expression of the myd88, Hc, Relish and proPO genes decreased in the gills during the 7-day recovery period. Exposure to nanoplastics for 48 h and recovery for 7 days significantly decreased the activities of lysozyme (LZM) alkaline phosphatase (AKP), total superoxide dismutase (SOD) and phenoloxidase (POD) and, glutathione peroxidase (GPX) in the hepatopancreas. Meanwhile, the relative abundance of pathogens exposed to 10 mg/L nanoplastics for 48 h increased at the species level, and these pathogens decreased significantly in the 7-day recovery period. These results suggested that exposure to nanoplastics for 48 h affected the activities of immune system enzymes and expression of immune-related genes in Eriocheir sinensis and altered the diversity and composition of their gut microbiota. E. sinensis could not recover from damage to the hepatopancreas within a 7-day recovery period. The results of this study provided insight into the effects of nanoplastics on crustaceans and it filled a gap in research on crustacean recovery after exposure to nanoplastics.
This study investigated the effects of nanoplastics (NPs) of varying particle sizes (75, 500, and 1000 nm) and concentrations (2.5 and 10 mg/L) on the gut health of Chiromantes dehaani. The experimental groups included a control (Cg0), and varying combinations of particle size and concentration. Our results showed that 75 nm NPs were more likely to enhance pathogenic bacterial growth than other sized NPs. Compared with CK, Low NPs concentrations (2.5 mg/L) raised total cholesterol (T-CHO) levels in the gut, while high concentrations significantly decreased both triglyceride (TG) and T-CHO levels (p
A comprehensive bioinformatics analysis was conducted to elucidate the innate immune response of Charybdis japonica following exposure to Aeromonas hydrophila. This study integrated metabolomics, 16S rRNA sequencing, and enzymatic activity data to dissect the immune mechanisms activated in response to infection. Infection with A. hydrophila resulted in an increased abundance of beneficial intestinal genera such as Photobacterium spp., Rhodobacter spp., Polaribacter spp., Psychrilyobacter spp., and Mesoflavibacter spp. These probiotics appear to suppress A. hydrophila colonization by competitively dominating the intestinal microbiota. Key metabolic pathways affected included fatty acid biosynthesis, galactose metabolism, and nitrogen metabolism, highlighting their role in the crab's intestinal response. Enzymatic analysis revealed a decrease in activities of hexokinase, phosphofructokinase, and pyruvate kinase, which are essential for energy homeostasis and ATP production necessary for stress responses. Additionally, reductions were observed in the activities of acetyl-CoA carboxylase and fatty acid synthase. Gene expression analysis showed downregulation in Peroxiredoxin 1 (PRDX1), Peroxiredoxin 2 (PRDX2), glutathione-S-transferase (GST), catalase (CAT), and glutathione (GSH), with concurrent increases in malondialdehyde (MDA) levels, indicating severe oxidative stress. This study provides insights into the molecular strategies employed by marine crabs to counteract bacterial invasions in their natural habitat.
Nano-plastics (NPs) have emerged as prevalent contaminants in aquatic ecosystems, gaining significant research interest. Nonetheless, limited research has addressed the toxicity mechanisms associated with PS-NPs (polystyrene nanoplastics) of varying particle sizes. In this investigation, genotoxicity, growth patterns, hepatopancreatic damage, and intestinal flora alterations in freshwater shrimp Neocaridina palmata (Shen 1948), subjected to 35 days PS-NPs exposure (two size PS-NPs: 75 nm and 200 nm were used for this experiment, and five concentrations were set: 0 mg/L, 0.5 mg/L, 2.5 mg/L, 5 mg/L, and 10 mg/L concentrations PS-NP concentrations were examined using RNA sequencing, histopathological analyses, enzyme activity assessments, and 16S rRNA sequencing. Noteworthy variations in differentially expressed genes (DEGs) were identified across groups exposed to different PS-NPs sizes. We observed that PS-NPs predominantly instigated cellular component-related processes and induced apoptosis and oxidative stress across tissues via the mitochondrial pathway. Although the 200 nm-PS-NPs are stronger than the 75 nm-PS-NPs in terms of fluorescence intensity, 75 nm-PS-NPs are more likely to promote apoptosis than 200 nm-PS-NPs. PS-NPs impeded standard energy provision in N. palmata, potentially contributing to decreased body length and weight. Moreover, PS-NPs inflicted damage on intestinal epithelial and hepatopancreatic tissues and significantly modified intestinal microbial community structures. Specifically, PS-NPs-induced intestinal damage was marked by a decline in some probiotics (notably Lactobacilli) and a surge in pathogenic bacteria. Moreover, supplementing N. palmata with Lactobacilli appeared ameliorate oxidative stress and strengthen energy metabolism. Our findings provided valuable insights into crustacean toxicity mechanisms when subjected to PS-NPs and the potential risks that different PS-NPs sizes posed to terrestrial ecosystems.
The extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5β1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5β1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5β1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases.