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Nanoplastics and di(2-ethylhexyl) phthalate (DEHP) are ubiquitous emerging contaminants that are transferred among organisms through food chain in the ecosystem. This study evaluated the trophic transfer of polystyrene nanoplastics (PSNPs) and DEHP in a food chain including Chlorella pyrenoidosa , Daphnia magna and Micropterus salmoides (algae-crustacean-fish) and lipid metabolism at a higher trophic level in fish. Our results showed that the PSNPs and DEHP accumulated in C. pyrenoidosa or D. magna were transferred to the M. salmoides , of which the DEHP were not biomagnified, while the PSNPs were trophically amplified by the food chain. It is suggested that more PSNPs might be accumulated by higher level consumers in a longer food chain. Additionally, the trophic transfer of PSNPs and DEHP resulted in antioxidant response and histopathological damage in M. salmoides. Moreover, the lipid biochemical parameters and lipid metabolism related genes (fasn , hsl , cpt1a , atgl , apob , fabp1 , lpl , cetp) of M. salmoides were significantly affected, which indicated disturbance of lipid metabolism. This study offers great insight into the transfer of contaminants by trophic transfer and their negative effects on organisms at higher trophic levels, which cause human exposure to MNPs and organic contaminants in the ecosystem. [Display omitted] • Trophic transfer of nanoplastics and di(2-ethylhexyl) phthalate by food chain. • PSNPs were trophically amplified through trophic transfer. • Trophic transfer of PSNPs and DEHP caused oxidative stress and damage of fish. • Trophic transfer of PSNPs and DEHP disturbed the lipid metabolism of fish. [ABSTRACT FROM AUTHOR]

• Polystyrene nanoplastics (PSNPs) significantly affected the growth and feed intake. • DEHP-PSNPs co-exposure significantly increased PSNPs retention in the intestines. • DEHP-PSNPs co-exposure caused significant oxidative stress and histological damages. • DEHP-PSNPs co-exposure changed the intestinal microbiota composition. Organic pollutants such as di-(2-ethylhexyl) phthalate (DEHP) interact with nanoplastics (NPs) and change their bioavailability and toxicity to aquatic organisms. This study aims to assess the ecotoxicological impacts of NPs in the presence and absence of DEHP on juvenile largemouth bass (LMB) Micropterus salmoides. Therefore, LMB was fed with diets containing various concentrations (0, 2, 10, and 40 mg/g) of polystyrene nanoplastics (PSNPs) by the weight of diets. After a 21-day of PSNPs dietary exposure, LMB was treated with DEHP at 450 μg/L through waterborne exposure for three days. Our results showed that PSNPs were accumulated in the intestinal tissues, which significantly decreased the feeding and growth rates in LMB. The histopathological analysis showed the intestine and liver of LMB were subjected to various degrees of structural damage caused by PSNPs, and DEHP-PSNP co-exposure enhanced those histopathological damages in both tissues. Additionally, the co-exposure induced oxidative stress in terms of increased activities of glutathione S-transferase, catalase, and superoxide dismutase enzymes in the liver, intestine, spleen, and serum. Furthermore, the co-exposure significantly changed the intestinal microbial composition, i.e., the decrease in the abundance of probiotics (Bacteroidetes and Proteobacteria) and the increase in pathogenic bacteria (Firmicutes) posed a great threat to fish metabolism and health. Therefore, this study highlights that the presence of DEHP enhances the toxicity of NPs on LMB in freshwater and suggests the regulated use of plastic and its additives for improving the health status of aquaculture fish for food safety in humans. [Display omitted] [ABSTRACT FROM AUTHOR]

The widespread distribution of micro(nano)plastics (MNPs) and bisphenols (BPs) in the environment inevitably resulted in their multifaceted interactions and associated detrimental effects being largely uncharted yet. Hence, this review summarized available studies highlighting the environmental occurrence, sorption mechanisms, and eco-toxicological effects of MNPs and BPs. The existing data indicated that the environmental concentrations of the adsorbed bisphenol A (BPA) and bisphenol S (BPS) on MNPs were 9.52–4961 ng/g and 1.89–118 ng/g of plastic particles, respectively, while bisphenol F (BPF) was below the detection limit. Hydrophobic interaction force was predominantly observed as the main factor in maintaining the adsorption of MNPs and BPA/S, whereas electrostatic repulsion between MNPs and BPF inhibited the adsorption of BPF onto plastic particles. Moreover, co-exposure to MNPs and BPs posed immune responses, neurotoxicity, reproductive inhibition and even survival impairment in test organisms. This review implied that it would facilitate the evaluation of the ecological safety and environmental risks of MNPs and BPs as well as contribute to theoretical guidance for their pollution prevention and control. To better understanding the associated toxicological mechanisms, there is an urgent need to assess the combined toxicological effects of MNPs and BPs. [Display omitted] • Hydrophobic interaction forces primarily maintain the adsorption of BPs on MNPs. • BPA alternatives are not environmentally friendly, they exhibit toxic impacts. • MNPs increased the reproductive toxicity of BPA to the test organisms. • Toxicogenetic mechanisms of MNPs and BPs and the factors affecting them are further required to clarify. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs) are emerging environmental contaminants with alarming ecological and human health concerns due to their unique physicochemical properties. This study elucidates the impacts of environmentally relevant concentrations (ERCs, 300 and 3000 ng/L) and sublethal concentrations (SLCs, 300 and 3000 μg/L) of polystyrene nanoplastics (PS-NPs, size 80 nm) on the intestinal immune response and gut microbiota of grass carp (Ctenopharyngodon idella). Exposure to SLCs showed greater accumulation of NPs in gut and gill tissue, and more pronounced gut damage (vacuolization of gut villi) compared to ERCs. SLCs significantly increased ROS levels with increasing exposure duration and exposure concentration (p < 0.05). In addition, SLCs significantly increased the transcription levels of several immune response-related genes such as IL-6 , IL-8 , IL-10 , IL-1β , and TNF-α (p < 0.05). However, the ERC exposure group at 3000 ng/L significantly increased the expression levels of IL-10 and TNF-α , compared to the control group (p < 0.05). Moreover, PS-NPs at both ERCs and SLCs significantly alter grass carp gut microbiota at the phylum and genus levels and disrupts microbial community composition and homeostasis (p < 0.05). At the phylum level, the abundance of Proteobacteria and Verrucomicrobiota was increased after PS-NPs exposure, while that of Spirochaetota and Fusobacteriota decreased. At the genus level, the number of beneficial bacteria decreased and the number of pathogenic bacteria increased. Our findings suggest that PS-NPs at the level of ERCs and SLCs can induce inflammation of the intestine and microbiota imbalance in grass carp. Our findings contribute to a deeper understanding of the gut toxicity of PS-NPs under environmentally relevant conditions in freshwater commercial fish. These experimental results suggest that PS-NPs may indirectly damage grass carp intestinal epithelium by modulating the gut microbiota, thereby damaging the grass carp gut. Hence, this study provides valuable hints on the intestinal barrier structure and functional damage mediated by NPs exposure. [Display omitted] • PS-NPs' effects at environmental & sublethal concentrations on grass carp were investigated. • SLCs induced higher PS-NPs accumulation in the gills and intestines. • SLCs caused higher oxidative stress and structural damage in intestinal tissues. • ERCs and SLCs produced similar changes in the microbiome composition. • Both ERCs and SLCs caused significant gut microbiota dysbiosis and inflammation. [ABSTRACT FROM AUTHOR]