Diazinon is a common organophosphate pesticide widely used to control parasitic infections in agriculture. Excessive use of diazinon can have adverse effects on the environment and aquatic animal health. In the present study, the toxic effects of diazinon on the histology, antioxidant, innate immune and intestinal microbiota community composition of crucian carp (Carassius auratus gibelio) were investigated. The results showed that diazinon at the tested concentration (300 μg/L) induced gill and liver histopathological damages. Hepatic total superoxide dismutase (T-SOD), catalase (CAT), and glutathione S-transferase (GST) activities significantly decreased (P < 0.05) by 32.47%, 65.33% and 37.34%, respectively. However, the liver tissue malondialdehyde (MDA) content significantly (P < 0.05) increased by 138.83%. The 300 μg/L diazinon significantly (P < 0.05) downregulated the gene expression of TLR4, MyD88, NF-kB p100 and IL-8 but had no significant effect TNF-α (P = 0.8239). In addition, the results demonstrated that diazinon exposure could affect the intestinal microbiota composition and diversity. Taken together, the results of this study indicated that diazinon exposure can cause damage to crucian carp, induce histopathological damage in gill and liver tissues, oxidative stress in the liver, and innate immune disorders and alter intestinal microbiota composition and diversity.

The crude e-waste recycling has been regulated in China since the late 2000s; however, information on the recent levels and the ecological risks of e-waste derived contaminants such as halogenated flame retardants (HFRs) in the e-waste sites are limited. We therefore examined the concentrations of several HFRs in wild, prey-sized mud carps collected from a typical e-waste site in 2006, 2011 and 2016, to understand the exposure dynamics and ecological risk of these chemicals. Several ecological and biological parameters including δ¹⁵N, δ¹³C, body size and lipid content of the fish were also examined, to ensure an overall uniformity of the sample set among the sampling years. Among the HFRs measured, polybrominated diphenyl ethers (PBDEs) were detected at the highest concentrations (contributing >90% to ∑HFRs), followed by Dechlorane Plus (DPs), polybrominated biphenyls (PBBs), and alternative brominated flame retardants (ABFRs). The fish concentrations of ∑PBDEs, ∑PBBs and ∑DPs significantly dropped by 65%, 57% and 53% from 2006 to 2011, and 12%, 74% and 51% from 2011 to 2016, respectively; likely reflecting the positive impact of the environmental regulations on crude e-waste recycling. The ∑ABFRs concentrations were also decreased by 80% from 2006 to 2011, but increased by 127% from 2011 to 2016; suggesting possible fresh input of these novel HFRs in recent years. In addition to the changes in the HFR concentrations, contaminant profiles in the fish were also changed, possibly due to environmental degradation of the HFRs. Despite our conservative method of risk assessment, we found that PBDEs posed an important risk both for the mud carp and for piscivorous wildlife that inhabit the e-waste site.

Although the toxicity of silver nanoparticles (AgNPs) in aquatic organisms has been extensively investigated, the mechanism by which AgNPs damage membranes remains unclear. This study investigated the toxic effects of a series of sub-lethal concentrations of AgNPs on the membranes of freshwater carp (Cyprinus carpio) gills, based on changes in membrane fatty acid (FA) profile, membrane fluidity, membrane lipid peroxidation, and histopathology. Most of the FAs in fish gill membrane was not significantly affected by exposure to multiple AgNPs concentrations, only few significant changes occurred in some specific FAs species at a high concentration of AgNPs exposure. In particular, high concentrations of AgNPs significantly decreased the proportions of two important long-chain n-3 series polyunsaturated FAs (C20: 5n3, and C22: 6n3), resulting in a decreased ratio of n-3 polyunsaturated FAs to n-6 polyunsaturated FAs (Σn-3UFA/Σn-6UFA). The AgNPs also caused a dose-dependent decrease in fish gill membrane fluidity, increased the level of lipid peroxidation, and inhibited Na+/K+-ATPase enzyme activity. Further histopathological examination revealed that exposure to AgNPs can cause toxic responses in the lamellae, including the thinning of the basement membrane, malformation, and inflammation. Together, the results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane. The findings contribute significantly to our understanding of nanoparticle-induced membrane toxicity and potential risks in aquatic environments.

Fish-associated antibiotic resistance genes (ARGs) have attracted increasing attention due to their potential risks to human beings via the food chain. However, data are scarce regarding the antibiotic resistance in fish themselves. Herein, the antibiotic resistance genes (ARGs) were assessed in the gut of four major Chinese freshwater carp (i.e., silver carp, grass carp, bighead carp, and crucian carp) from food retail markets. Results show that the abundances of target ARGs (e.g., tetA, tetO, tetQ, tetW, sulI, sulII, and blaTEM₋₁) and class 1 integrase (intI1) were in the range 9.4 × 10⁻⁶ - 1.6 × 10⁻¹ and 6.7 × 10⁻⁵ - 5.2 × 10⁻² gene copies per 16S rRNA gene, respectively. The sulI, sulII, and tetQ strongly correlated with silver and mercury resistance genes (e.g., silE and merR). The microbial taxa of fish gut could be partly separated among retail markets based on the PCA analysis. About 15.0% of the OTUs in fish gut were shared and 74.5% of the shared OTUs were identified as Acidobacteria, Bacteroidetes, Chloroflexi, Cyanobacteria, Firmicutes, and Proteobacteria. These phyla may constitute the core microbiota in the guts of the four Chinese freshwater carp. The possible ARG hosts were revealed based on the network analysis, and the presence of pathogen-associated resistant genera in fish gut highlights the need to fully understand their potential human health risks.

This study evaluated the effect of growth of different tissue compartments on the bioaccumulation of mercury (Hg) and polychlorinated biphenyls (PCBs) in Silver Carp (Hypophthalmichthys molitrix) and Bighead Carp (Hypophthalmichthys nobilis) from the Three Gorges Reservoir (TGR), China. A non-steady state bioenergetics/toxicokinetic model was developed to simulate PCB and Hg concentrations in these two species and compared with field data. Simulations using constant whole body growth rate and constant tissue to whole body weight ratios were contrasted against simulations adopting age specific whole body and tissue/age specific growth rates for their goodness of fit to field data. The simulations using age/tissue specific growth rates demonstrated better fit to field data for PCBs compared to the constant growth rate models (22% improved R²), while both models explained similar variation in Hg concentration data. Both species demonstrated higher growth rates of lipids (on a daily basis) relative to whole body and protein contributing to higher growth dilution of PCBs compared to Hg. Although stable isotope data indicated some degree of diet and/or habitat shift, simulations assuming a constant diet concentration explained between 36 and 40% of the variation in fish concentrations for both contaminants and fish species. This study demonstrates that differences in the bioaccumulation rate of PCBs and Hg by Asian carp can be partially explained by differences in the growth rates of key tissue storage compartments associated with each contaminant. These differences in chemical-specific growth dilution subsequently contribute to differences in chemical retention and bioaccumulation patterns of Hg and PCBs by fish.

Information on tissue distribution of Dechlorane Plus (DP) and its dechlorinated analogs in wildlife is scarce. DP isomers and two dechlorinated compounds, anti-Cl₁₁-DP and anti-Cl₁₀-DP, were examined in the muscle, liver, and brain tissues of two bottom fish species collected from an electronic waste recycling site, South China. The median levels of syn-, anti-, and anti-Cl₁₁-DP isomers in the tissues ranged 0.18–39.1, 0.22–52.9, and 0.01–5.63 ng/g wet wt, respectively. Anti-Cl₁₀-DP was only detected in one muscle sample of mud carp (0.01 ng/g wet wt), although it was consistently detected in the sediments (0.42–0.83 ng/g dry wt). Preferential distribution in liver relative to muscle was observed for syn-DP and anti-Cl₁₁-DP. However, a high persistent retention in the brain compared to the liver was observed for anti-DP, suggesting that this isomer can across the blood–brain barrier of fish, and may cause adverse effects to the nervous system in the exposed biota.

In this study, the influence of the co-existence of TiO2 nanoparticles on the speciation of arsenite [As(III)] was studied by observing its adsorption and valence changing. Moreover, the influence of TiO2 nanoparticles on the bioavailability of As(III) was examined by bioaccumulation test using carp (Cyprinus carpio). The results showed that TiO2 nanoparticles have a significant adsorption capacity for As (III). Equilibrium was established within 30 min, with about 30% of the initial As (III) being adsorbed onto TiO2 nanoparticles. Most of aqueous As (III) was oxidized to As(V) in the presence of TiO2 nanoparticles under sunlight. The carp accumulated considerably more As in the presence of TiO2 nanoparticles than in the absence of TiO2 nanoparticles, and after 25-day exposure, As concentration in carp increased by 44%. Accumulation of As in viscera, gills and muscle of the carp was significantly enhanced by the presence of TiO2 nanoparticles. The co-existence of TiO2 nanoparticles could change the speciation of arsenite by adsorption and photo-oxidation, and enhance its bioaccumulation to carp.

Water, sediment, and wild aquatic species were collected from an electronic waste (e-waste) polluted pond in South China. This study aimed to investigate the bioaccumulation, tissue distribution, and trophic transfer of organophosphorus flame retardants (PFRs) in these aquatic organisms. The concentrations of PFRs detected in the analyzed organisms were between 1.7 and 47 ng/g wet weight (ww). Oriental river prawn and snakehead exhibited the highest and lowest levels, respectively. Tri-n-butyl phosphate (TnBP), tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) phosphate (TCPP) and triphenyl phosphate (TPhP) were dominant contaminants, accounting for approximately 86% of the total sum. The mean values of bioaccumulation factors (BCFs) and logarithmic biota-sediment accumulation factors (log BSAFs) for individual PFRs varied from 6.6 to 1109 and from −2.0 to 0.41, respectively. Both log BCFs and log BSAFs of PFRs were significantly and positively correlated with their octanol-water partitioning coefficient (log KOW). The concentrations of PFRs in tissues of large mud carp and snakehead were significantly and positively correlated with the lipid content (each p < 0.05) and the liver, kidney, and gill exhibited high PFR levels. When the concentration was expressed on a lipid basis, liver exhibited the lowest level, indicating the probable effects of metabolism. Significantly positive correlation was also found between lipid content and total PFR concentration in muscle of all aquatic organisms, given the strong correlation between lipid content and the concentration of TnBP. Trophic magnification factors (TMF) of TnBP and TPhP were lower than 1 (0.57 and 0.62), indicating that these PFRs undergo trophic dilution in this aquatic food web.

In this study, we aimed to identify the toxic effects of chlorpyrifos exposure on the tissues of common carp. For this purpose, we evaluated histopathological changes in the brain, gills, liver, kidney, testis, and ovaries after 21 days of chlorpyrifos exposure. Activation of 8-OHdG, cleaved caspase-3, and iNOS were assesed by immunofluorescence assay in chlorpyrifos-exposed brain and liver tissue. Additionally, we measured the expression levels of caspase-3, caspase-8, iNOS, MT1, CYP1A, and CYP3A genes in chlorpyrifos-exposed brain tissue, as well as the expression levels of FSH and LH genes in chlorpyrifos-exposed ovaries, using qRT-PCR. We observed severe histopathological lesions, including inflammation, degeneration, necrosis, and hemorrhage, in the evaluated tissues of common carp after both high and low levels of exposure to chlorpyrifos. We detected strong and diffuse signs of immunofluorescence reaction for 8-OHdG, iNOS, and cleaved caspase-3 in the chlorpyrifos-exposed brain and liver tissues. Furthermore, we found that chlorpyrifos exposure significantly upregulated the expressions of caspase-3, caspase-8, iNOS, and MT1, and also moderately upregulated CYP1A and CYP3A in the brain tissue of exposed carp. We also noted downregulation of FSH and LH gene expressions in chlorpyrifos-exposed ovary tissues. Based on our results, chlorpyrifos toxication caused crucial histopathological lesions in vital organs, induced oxidative stress, inflammation, and apoptosis in liver and brain tissues, and triggered reproductive sterility in common carp. Therefore, we can propose that chlorpyrifos toxication is highly dangerous to the health of common carp. Moreover, chlorpyrifos pollution in the water could threaten the common carp population. Use of chlorpyrifos should be restricted, and aquatic systems should be monitored for chlorpyrifos pollution.