Aquatic Toxicology最新文献

Accidental oil spills into the ocean can lead to downward transport and settling of oil onto the seafloor as part of marine snow, as seen during the Deepwater Horizon incident in 2010 in the Gulf of Mexico. The arctic and subarctic regions may favor conditions leading to this benthic oil deposition, prompting questions about the potential impacts on benthic communities. This study investigated the effects of oil-contaminated marine snow uptake on the blue mussel (Mytilus sp.). We exposed mussels for four days to 1) oil-contaminated marine snow (MOS treatment), or to 2) chemically-enhanced water-accommodated fraction (CEWAF) of oil plus unaggregated food particles (CEWAF treatment). Both oil treatments received the same nominal concentration of oil and food. Two controls were included: 1) Clean seawater plus unaggregated food (agg-free control) and 2) clean seawater plus marine snow (marine snow control). After the exposure, mussels were allowed to recover for ten days under clean, running seawater. Samples were taken right before and after the exposure period, and after the recovery phase for the following endpoints: distribution (partitioning) of oil compounds between seawater and MOS, and between seawater and mussel tissue; DNA damage (assessed via the comet assay); clearance rate; and condition index [tissue dry weight (g) divided by shell length (mm)]. Some discernable patterns were found in the partitioning of oil compounds between seawater and MOS. However, these patterns did not translate to any significant differences in the partitioning of oil compounds into mussel tissue between the two oil treatments. DNA damage did not exceed background levels (10% tail DNA or less; to be expected in healthy, viable cells) at any sampling time point, but significantly higher DNA damage was observed in CEWAF-T compared to MOS-T mussels after the recovery phase. After the exposure, a significant difference emerged in the clearance rate between the CEWAF treatment and the agg-free control, but not between the MOS treatment and the marine snow control. All mussels except those from the CEWAF treatment exhibited an increased condition index after the exposure time. Together, these results suggest that aggregates could moderate the effects of oil exposure on blue mussels, possibly by providing better, more concentrated nutrition than unaggregated food particles.

This study aimed to investigate the protective effects of Allium jesdianum essential oil (AJEO) in decreasing cypermethrin toxicity for rainbow trout. First, the safety of the 0%, 0.5%, 1%, and 1.5% AJEO supplements was assayed after 60 days. Then, the protective effects of AJEO were studied on fish exposed to 12.5% 96h LC50 cypermethrin after 14 days. Results showed that 1 and 1.5% AJEO administration enhanced protease and lipase activities in the intestine and improved growth performance. Moreover, feeding fish with 1 and 1.5% AJEO increased catalase (CAT) and superoxide dismutase activities (SOD) and decreased malondialdehyde (MDA). Also, AJEO increased glutathione peroxidase (GPx) activity in serum. However, exposure to cypermethrin significantly decreased these enzyme activities and increased MDA. The oxidative biomarkers remained normal in fish fed with AJEO after exposure to cypermethrin. The administration of 1 and 1.5% AJEO significantly decreased cortisol and glucose levels, alkaline phosphatase (ALP), lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase activities. Although exposure to cypermethrin significantly increased these biochemical biomarkers, AJEO could adjust them. A significant effect of 1% AJEO on total protein and globulin was observed before and after exposure to cypermethrin. Exposure to cypermethrin decreased all immunological parameters in the serum and mucus. However, administration of 1% AJEO increased protease, lysozyme (LYS) activities, total immunoglobulin (Ig), complement C3 and C4, and nitroblue tetrazolium (NBT) in the serum and ALP, LYS, protease activities and Ig in mucus. In conclusion, results showed that AJEO could potentially decrease the toxicity effects of cypermethrin in fish.

Glyphosate, a prevalent herbicide, has raised concerns due to its potential ecological impact, especially on aquatic ecosystems. While it is crucial for managing agricultural productivity, its inadvertent effects on non-target aquatic species like the red swamp crayfish, Procambarus clarkii, are not fully understood. In the present study, the neurotoxicity, oxidative stress, and immune suppression of glyphosate on P. clarkii were investigated. Sublethal glyphosate exposure (5, 10 and 20 mg/L) for 96 h was found to significantly decrease AChE activity in both brain and hepatopancreas, correlating with reduced foraging efficiency and increased turnover time. Oxidative stress was evident through increased lipid peroxidation (LPO) and malondialdehyde (MDA) levels and altered antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). In addition, the total antioxidative capacity (T-AOC) was inhibited at 10 and 20 mg/L of glyphosate exposure. Immune assays revealed a decrease in total hemocyte counts (THC) and suppression of key immune enzyme activities and transcriptional expressions at higher concentrations, suggesting compromised immune defenses. The findings demonstrate that glyphosate can induce considerable neurotoxic and immunotoxic effects in P. clarkii, disrupting essential physiological functions and behavior.

In this study, the impact of ammonia nitrogen stress on juvenile four-finger threadfin in pond culture was examined. The 96-hour median lethal concentration (LC50-96h) and safe concentration of ammonia nitrogen were assessed in juveniles with a body weight of 7.4 ± 0.6 g using ecotoxicological methods. The study design included a stress group exposed to LC50-96h levels of ammonia nitrogen and a control group without ammonia nitrogen exposure. To examine the physiological, biochemical, and metabolic effects of ammonia nitrogen on gill tissue, gill tissue samples were collected after 12, 24, 48, and 96 h of stress, with a resumption of treatment after 48 h. Compared to the control group, ammonia nitrogen adversely affected juvenile four-finger threadfin, with LC50-96h and safe concentration values of 20.70 mg/L and 2.07 mg/L, respectively. Exposure to ammonia nitrogen resulted in substantial gill damage, including fusion of lamellae, epithelial cell loss, and proliferation of chlorine-secreting cells. This tissue damage persisted even after a 48-h recovery period. Ammonia nitrogen stress triggered an increase in antioxidant enzyme activity (superoxide dismutase, catalase, and glutathione peroxidase) and malondialdehyde levels in gills, indicating oxidative stress from 12 h onwards. Although enzyme activity decreased over time, oxidative stress persisted even after recovery, suggesting an ongoing need for antioxidant defense. Metabolomics analysis showed significant alterations in 423 metabolites under ammonia nitrogen stress. Key metabolites such as L-arginine, taurine, 20-hydroxyarachidonic acid, 11,12-dihydroxy-5Z, 8Z, and 14Z eicosotrienic acid followed an increasing trend; uridine, adenosine, L-glutathione, and thymidine 5′-triphosphate followed a decreasing trend. These changes reflect metabolic adaptations to stress. In enriched metabolic pathways, the main differential pathways are membrane transport, lipid metabolism, and amino acid metabolism. After 48 h, significant differences were observed in 396 metabolites compared to the control group. Notably, L-arginine, choline, and L-histidine increased, while linoleic acid, adenosine, and glutathione decreased. Amino acid and lipid metabolism pathways were key affected pathways. Under ammonia nitrogen stress, juvenile four-finger threadfin increased the synthesis of unsaturated and saturated fatty acids to cope with low temperatures and bolster immune function by consuming spermidine. This adaptation helps to clear peroxides generated during fatty acid synthesis, thereby protecting cells from oxidative damage. This study provides insights for pond aquaculture and breeding of ammonia nitrogen-tolerant fish strains.

Residues of human pharmaceuticals are widely detected in surface waters and can be taken up by and bioaccumulate in aquatic organisms, especially fish. One of the key challenges in assessing the bioaccumulation potential of ionizable organic compounds, such as the pharmaceuticals, is the lack of empirical data for biotransformation. In the present study, we assessed the in vitro intrinsic clearances (CL_INT) of twelve pharmaceuticals, individually and some additionally as mixtures, in rainbow trout (Oncorhynchus mykiss) liver S9 fractions (RT-S9) adhering to the OECD test guidance 319B. The test substances included four anti-inflammatory agents (diclofenac, ibuprofen, ketoprofen, naproxen), seven antidepressants/antipsychotics (citalopram, haloperidol, levomepromazine, mirtazapine, risperidone, sertraline, venlafaxine) and the O-desmethyl metabolite of venlafaxine. Quantifiable intrinsic clearances were detected for diclofenac, ibuprofen, naproxen, levomepromazine, and sertraline. Apart from diclofenac, the in vitro clearances of the other four pharmaceuticals were shown to be critically dependent on the cytochrome P450 (CYP) metabolism. Therefore, we also determined the half-maximal inhibitory concentrations (IC₅₀) of the same twelve pharmaceuticals toward CYP1A-like (7-ethoxyresorufin-O-deethylation, EROD) and CYP3A-like (benzyloxy-4-trifluoromethylcoumarin-O-debenzyloxylation, BFCOD) activities in RT-S9 using IC₅₀ shift assay. As a result, levomepromazine and sertraline were identified as the most potent inhibitors of both EROD and BFCOD activity (unbound IC₅₀ < 10 µM each), followed by citalopram and haloperidol (10 µM < IC₅₀ < 100 µM). Additionally, mirtazapine was a selective EROD inhibitor (IC₅₀ ∼ 30 µM). The inhibitory impacts of haloperidol and sertraline were indicatively time dependent. Finally, we carried out intrinsic clearance assays with mixtures of diclofenac, ibuprofen, naproxen, levomepromazine, and sertraline to examine the impacts of EROD and BFCOD inhibitions on their in vitro CL_INT in RT-S9. Our in vitro data suggests that the intrinsic clearances of ibuprofen, levomepromazine, and sertraline in rainbow trout can be significantly reduced as the result of P450 inhibition by pharmaceutical mixtures, whereas the clearances of diclofenac and naproxen are less impacted.

The global prevalence and accumulation of plastic waste is leading to pollution levels that cause significant damage to ecosystems and ecological security. Exposure to two concentrations (1 and 5 mg/L) of 500 nm polystyrene (PS)-nanoplastics (NPs) for 14 d was evaluated in Simocephalus vetulus using transcriptome and 16 s rRNA sequencing analyses. PS-NP exposure resulted in stress-induced antioxidant defense, disturbed energy metabolism, and affected the FoxO signaling pathway, causing neurotoxicity. The expression of Cyclin D1 (CCND), glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxykinase (PCK) genes was decreased compared to the control, whereas the expression of caspase3 (CASP3), caspase7 (CASP7), Superoxide dismutase (SOD), Heat shock protein 70 (HSP70), MPV17, and Glutathione S-transferase (GST) genes was increased, thus, suggesting that NP ingestion triggered oxidative stress and disrupted energy metabolism.. PS-NPs were present in the digestive tract of S. vetulus after 14 days of exposure. In addition, the abundance of the Proteobacteria and opportunistic pathogens was elevated after PS-NPs exposure. The diversity and homeostasis of the S. vetulus gut microbiota were disrupted and the stability of intestinal barrier function was impaired. Multiomic analyses highlighted the molecular toxicity and microbial changes in S. vetulus after exposure to NPs, providing an overview of how plastic pollution affects freshwater organisms and ecosystems.

Recently, nano-titanium dioxide (nano-TiO₂) has been widely distributed over surface water. However, there are few reports on its effects on the central nervous system of fish. In this study, we investigated whether nano-TiO₂ enters the medaka brain after exposure and its effect on the brain. Marine medaka brains were examined after exposure to 0.01 g/L nano-TiO₂ for 3, 10, and 20 d. Nano-TiO₂-like particles were found in the telencephalon of treated fish. There was no obvious brain histopathological injury. The number of irregular mitochondria with absent cristae increased. Gene expression of the apoptosis-related genes, casp8, bcl2b, and bax, decreased significantly in the nano-TiO₂ group at 3 d. In contrast, the pyroptosis-related genes, gsdmeb and casp1, and inflammation-related factor, il18, increased significantly. As an activated microglia marker, mRNA expression of cd68 increased significantly in the nano-TiO₂ treated group. Moreover, CD68 protein expression also increased significantly at 10 d. Altogether, we show that nano-TiO₂ can alter mitochondrial morphology in the telencephalon of medaka, leading to microglial activation and pyroptosis.

Nano-TiO₂ is inevitably released into aquatic environment with increasing of nanotechnology industries. Study pointed that different individuality showed divergent behavioral and physiological response when facing environmental stress. However, the effects of nano-TiO₂ on tolerance of bivalves with different individualities remain unknown. In the study, clams were divided into two types of individuality - proactive and reactive by post-stress recovery method. It turned out that proactive individuals had quicker shell opening level, stronger burrowing behavior, faster feeding recovery, higher standard metabolic rate and more rapid ammonia excretion ability than reactive individuals after exposed to air. Then, the survival rate, hemocytes response and oxidase activity of classified clams were evaluated after nano-TiO₂ exposure. Results showed that after 30 d exposure, proactive individuals accelerated burrowing behavior with higher survival rate. Moreover, proactive clams had better adaptability and less hemocytes response and oxidative damage than reactive clams. The study highlights the individualities of marine shell fish determine individual capacity to adapt to environmental changes, play important roles in aquaculture and coastal ecosystem health.

Bisphenol S (BPS) is extensively utilized in various industries such as plastic manufacturing, food packaging, and electronics. The release of BPS into aquatic environments has been observed to have negative impacts on aquatic ecosystems. Research has shown that exposure to BPS can have adverse effects on the health of aquatic animals. This study aimed to explore the mechanism of oxidative stress and endoplasmic reticulum stress induced in freshwater crayfish (Procambarus clarkii) by exposure to BPS (0 µg/L, 1 µg/L, 10 µg/L, and 100 µg/L) for 14 days. The results showed that BPS exposure resulted in elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and severe intestinal histological damage. In addition, oxidative stress can occur in the body by inhibiting the activity of antioxidant enzymes and the expression of related genes. BPS exposure induced a significant increase in the relative mRNA expression levels of inflammatory cytokines (NF-κB and TNF-α) and key unfolded protein response (UPR) related genes (Bip, Ire1, and Xbp1). At the same time, BPS exposure also induced up-regulation of apoptosis genes (Cytc and Casp3), suggesting that UPR and Nrf2-Keap1 signaling pathways may play a protective role in the process of apoptosis and oxidative stress. In conclusion, Our findings present the initial evidence that exposure to environmentally relevant levels of BPS can lead to intestinal injury through various pathways, highlighting concerns about the potential harm at a population level from BPS and other bisphenol analogs.

Cadmium (Cd) poses significant risks to aquatic organisms due to its toxicity and ability to disrupt the cellular processes. Given the similar atomic radius of Cd and calcium (Ca), Cd may potentially affect the Ca homeostasis, which can lead to impaired mineralization of skeletal structures and behavioral abnormalities. The formation of the spinal skeleton involves Ca transport and mineralization. In this study, we conducted an in-depth investigation on the effects of Cd at environmental concentrations on zebrafish (Danio rerio) skeletal development and the underlying molecular mechanisms. As the concentration of Cd increased, the accumulation of Cd in zebrafish larvae also rose, while the Ca content decreased significantly by 3.0 %−57.3 %, and vertebral deformities were observed. Transcriptomics analysis revealed that sixteen genes involved in metal absorption were affected. Exposure to 2 µg/L Cd significantly upregulated the expression of these genes, whereas exposure to 10 µg/L resulted in their downregulation. Consequently, exposure of zebrafish larvae to 10 µg/L of Cd inhibited the body segmentation growth and skeletal mineralization development by 29.1 %−56.7 %. This inhibition was evidenced by the downregulation of mineral absorption genes and decreased Ca accumulation. The findings of this study suggested that the inhibition of skeletal mineralization was likely attributed to the disruption of mineral absorption, thus providing novel insights into the mechanisms by which metal pollutants inhibit the skeletal development of fish.