Polystyrene nanoplastics sequester the toxicity mitigating potential of probiotics by altering gut microbiota in grass carp (Ctenopharyngodon idella).

This study evaluated the role of probiotics in enhancing intestinal immunity and mitigating polystyrene nanoplastics (PS-NPs)-induced toxicity in grass carp (Ctenopharyngodon idella). Grass carp were fed probiotics (Bacillus subtilis, Bacillus velezensis, Lactobacillus reuteri, and Lactococcus lactis) for two weeks before being exposed to PS-NPs for five days. Probiotic pretreatment alleviated PS-NPs-induced intestinal damage, with Bacillus velezensis and Lactococcus lactis groups showing milder vacuolation and villus breakage than other groups. Probiotic-treated fish exhibited transient increases in antioxidant enzyme activities (CAT, SOD, MPO) and immune gene expression (IL-6, IL-8, IL-10, IL-1β, TNF-α, and IFN-γ2) shortly after exposure, followed by significant downregulation over time. Higher abundance of the gut dominant phylum Proteobacteria was observed in four probiotic groups exposed to PS-NPs than that in the blank control group. The Clostridium phylum showed a significant decrease in the abundance both in the LRS-PS100 and LLS-PS100 groups, while the abundance of the Thick-walled phylum increased. The Spearman correlation matrix revealed that specific gut microbiota, such as Serratia, Neisseria, and Lactococcus, were significantly associated with enzymatic activities and immune system related genes' expressions. Probiotic pretreatment enhanced the intestinal immune response of grass carp. However, this enhanced immune response was insufficient to counteract the toxic effects of PS-NPs exposure, particularly in terms of oxidative stress levels and gut microbial diversity. This study offers new insights into the potential of probiotics to combat NPs pollution in aquaculture. It emphasizes the need for further research to explore various probiotic combinations. Future studies should also investigate optimal dosages and durations to effectively mitigate the biological toxicity of NPs pollution.

Li Z ，Chen F ，Liu J ，Zhi L ，Junaid M ，Chen G ，Xiao Z ，Wang J ，Chong Y ... -  《-》

Erratum: Eyestalk Ablation to Increase Ovarian Maturation in Mud Crabs.

《Jove-Journal of Visualized Experiments》

Ecotoxicological effects of polystyrene nanoplastics on common carp: Insights into blood parameters, DNA damage, and gene expression.

Acar Ü ，İnanan BE ，Zemheri-Navruz F 《-》

Integration of physiology, microbiota and metabolomics reveals toxic response of zebrafish gut to co-exposure to polystyrene nanoplastics and arsenic.

Both nanoplastic (NP) particles and arsenic (As) are widespread in aquatic environments and pose a combined risk of exposure to aquatic organisms. How the gut of aquatic organisms responds to combined risk of exposure is still unclear. In this study, zebrafish (Danio rerio) were subjected to three distinct As stress environments: only As group (10 μg/L), and As combined with different concentrations of polystyrene (PS) NPs (1 mg/L and 10 mg/L) groups for 21 days via semi-static waterborne exposure. The physiological responses to combined stress, the diversity of gut microorganisms, and the metabolomic response of the gut were investigated. The findings indicated that PSNPs were prevalent in the intestines of zebrafish in the co-exposed group. Furthermore, the administration of 1 mg/L and 10 mg/L of PSNPs in the co-exposed group was observed to elevate As levels in the intestines by 24.88% and 76.95%, respectively, in comparison to As treatment alone. Simultaneous exposure of the gut to PSNPs and As resulted in increased contents/activities of MDA, SOD, CAT, and GST, and a decrease in contents/activities of GSH and GPx, when compared to As exposure alone. Additionally, the combined exposure led to an elevated expression of the Cu/Zn-sod, Mn-sod, gpx, and cat genes. The combined treatment with NPs and As resulted in an increase in the abundance of Proteobacteria and Fusobacteriota at the phylum level, as well as a significant increase in the abundance of Cetobacterium, Rhodococcus, and Bacteroides at the genus level. Non-targeted metabolomics analyses suggest that metabolic pathways affected by co-exposure include glycerophospholipid metabolism, glycerolipid metabolism, ABC transporters and autophagy. The findings of this study are of considerable significance for the evaluation of the toxicological impact of co-existing pollutants.

Li G ，Lv M ，Yu H ，Zhang H ，Zhang D ，Li Q ，Wang L ，Wu Y ... -  《-》

Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage.

Nanoplastics (NPs) have attracted widespread attention owing to their presence in the body. Recent studies highlighted the detrimental effects of NPs on the digestive tract. However, no studies have reported an association between NPs exposure and colitis-associated cancer (CAC). An azoxymethane/dextran sodium sulfate-induced CAC model was used, and polystyrene nanoparticles (PS-NPs) were selected for long-term exposure. Non-targeted metabolomics and 16S rRNA sequencing were used to detect changes in colonic metabolites and gut microbes following PS-NPs exposure. A lipopolysaccharide (LPS)-treated cancer cell model (Caco-2) exposed to PS-NPs was used to investigate the underlying molecular mechanism. Compared to the normal control group, mice in the PS-NPs group exhibited more tumor nodes and reactive oxygen species (ROS), higher expression of pan-CK and Ki-67, and more severe DNA damage. 16S rRNA sequencing revealed that exposure to PS-NPs altered the abundance of Allobaculum and Lactobacillus, whereas metabolic analysis showed that the most significant metabolites were enriched mostly in fatty acid metabolism. Experiments in LPS intervened Caco-2 cells showed that exposure to PS-NPs led to lipid peroxidation, oxidative stress, and DNA damage in Caco-2. Exposure to PS-NPs activated the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway both in the AOM/DSS mouse model and cellular model. Key proteins involved in fatty acid metabolism were downregulated in Caco-2 cells exposed to PS-NPs. The metabolic effects of cancer cells exposed to PS-NPs were significantly inhibited by the activation of the fatty acid metabolism pathway by fenofibrate. PS-NPs exposure disturbed lipid metabolism and induced DNA damage via the activation of PI3K/AKT/mTOR to promote CAC progression. Inhibition of fatty acid metabolism is a therapeutic target for controlling PS-NP-induced CAC. Our study provides an important reference for the prevention and treatment of CAC from the perspective of the environment and enhances awareness of the necessity of plastic control.

Tian S ，Li R ，Li J ，Zou J ... -  《-》