Aquatic Toxicology最新文献

This study examined the impact of sertraline, an antidepressant common in treated wastewater, on the host-parasite dynamics between parasitic freshwater mussel (Unio tumidus, Unionidae) larvae (glochidia) and their host fish (Squalius cephalus, Cyprinidae). Employing a full-factorial design, both fish and glochidia were subjected to sertraline at the combinations of 0 µg L⁻¹ (control), 0.2 µg L⁻¹ (environmentally relevant concentration), and 4 µg L⁻¹ (elevated concentration, short-term exposure of the parasite). The results showed that long-term host exposure (involving intensive sertraline accumulation in the fish brain) marginally increased subsequent glochidia attachment success by 2 %, while parasite exposure at the same environmentally relevant concentrations had no detectable effect. There was also no effect of exposure of glochidia to 0.2 µg L⁻¹ of sertraline on their viability and encapsulation success during the initial parasitic stage. However, a significant alteration in attachment behavior, marked by a 3.3 % increase in attachment success and changes in the glochidia spatial distribution on the host body, was noted after 24 h of glochidia exposure to 4 µg L⁻¹ of sertraline. Importantly, this study provides the first evidence of sertraline transfer from exposed glochidia to nonexposed host fish, as indicated by elevated levels of sertraline (12.8 ng g⁻¹) in the brain tissue of nonexposed hosts. These findings highlight the subtle yet significant effects of pharmaceutical pollutants on freshwater ecosystems but also underscore the importance of understanding the unexpected dynamics of such contamination to predict and address future ecological changes.

Environmental estrogens (EEs) are found extensively in natural waters and negatively affect fish reproduction. Research on the reproductive toxicity of EEs mixtures in fish at environmentally relevant concentrations is scarce. In this study, adult male zebrafish were exposed for 60 days to EES (a mixture of EEs), EE2-low (5.55 ng/L, with an estrogenic potency equal to EES), and EE2-high (11.1 ng/L). After exposure, the expression levels of vtg1, vtg3, and esr1 in the livers in EES-treated fish remained unaltered, whereas they were significantly increased in EE2-treated fish. Both EE2-high and EES exposures notably reduced the gonad somatic index and sperm count. A disrupted spermatogenesis was also observed in the testes of EE2-high- and EES-exposed fish, along with an alteration in the expression of genes associated with spermatogonial proliferation (pcna, nanog), cell cycle transition (cyclinb1, cyclind1), and meiosis (aldh1a2, cyp26a1, sycp3). Both EE2 and EES significantly lowered plasma 11-ketotestosterone levels in males, likely by inhibiting the expression level of genes for its synthesis (scc, cyp17a1 and cyp11b2), and increased 17β-estradiol (E2) levels, possibly through upregulating the expression of cyp19a1a. A significant increase in tnfrsf1a expression and the tnfrsf1a/tnfrsf1b ratio in EE2-high and EES-treated males also suggests increased apoptosis via the extrinsic pathway. Further investigation showed that both EE2-high and EES diminished the sexual behavior of male fish, accompanied with reduced E2 levels in the brain and the expression of genes in the kisspeptin/gonadotropin-releasing hormone system. Interestingly, the sexual behavior of unexposed females paired with treated males was also reduced, indicating a synergistic effect. This study suggests that EES have a more severe impact on reproduction than EE2-low, and EEs could interfere not only with spermatogenesis in fish, but also with the sexual behaviors of both exposed males and their female partners, thereby leading to a more significant disruption in fish reproduction.

Phenytoin, an antiepileptic drug, induces neurotoxicity and abnormal embryonic development and reduces spontaneous locomotor activity in fish. However, its effects on other endpoints remain unclear. Therefore, we investigated the effects of phenytoin on the swimming behavior and reproductive ability of Japanese medaka. Abnormalities in swimming behavior, such as imbalance, rotation, rollover, and vertical swimming, were observed. However, when phenytoin exposure was discontinued, the behavioral abnormality rates decreased. Phenytoin exposure also significantly reduced reproductive ability. By investigating reproduction-related gene expression of gnrh1, gnrh2, fshb, and lhb remained unchanged in males and females. In contrast, kiss1 expression was significantly suppressed due to phenytoin exposure in males and females. kiss2 expression was also significantly suppressed in females but not in males. We filmed videos to examine phenytoin exposure effects on sexual behavior. Females showed no interest in the male's courtship. As the kisspeptin 1 system controls sexual behavior in Japanese medaka, phenytoin exposure may have decreased kiss1 expression, which decreased female reproductive motivation; hence, they did not spawn eggs. This is the first study to show that phenytoin exposure induces behavioral abnormalities, and suppresses kiss1 expression and reproductive performance in Japanese medaka.

Avermectin, a widely used deworming drug, poses a significant threat to fisheries. Silybin is recognized for its antioxidant and anti-inflammatory properties. The kidney, being crucial for fish survival, plays a vital role in maintaining ion balance, nitrogen metabolism, and hormone regulation. While residual avermectin in water could pose a risk to carp (Cyprinus carpio), it remains unclear whether silybin can alleviate the renal tissue toxicity induced by avermectin in this species. In current study, we developed a model of long-term exposure of carp to avermectin to investigate the potential protective effect of silybin against avermectin-induced nephrotoxicity. The results indicated that avermectin induced renal inflammation, oxidative stress, ferroptosis, and autophagy in carp. Silybin suppressed the mRNA transcript levels of pro-inflammatory factors, increased catalase (CAT) activity, reduced glutathione (GSH) activity, diminished reactive oxygen species (ROS) accumulation in renal tissues, and promoted the activation of the Nrf2-Keap1 signaling pathway. Furthermore, the transcript levels of ferroptosis-associated proteins, including gpx4 and slc7a11, were significantly reduced, while those of cox2, ftl, and ncoa4 were elevated. The transcript levels of autophagy-related genes, including p62 and atg5, were also regulated. Network pharmacological analysis revealed that silybin inhibited ROS accumulation and mitigated avermectin-induced renal inflammation, oxidative stress, ferroptosis, and autophagy in carp through the involvement of PPAR-γ. Silybin exerted its anti-inflammatory effect through the NF-κB pathway and antioxidant effect through the Nrf2-Keap1 pathway, induced renal cell iron efflux through the SLC7A11/GSH/GPX4, and suppressed autophagy initiation via the PI3K/AKT pathway. This study provides evidence of the protective effect of silybin against avermectin-induced nephrotoxicity in carp, highlighting its potential as a therapeutic agent to alleviate the adverse effects of avermectin exposure in fish.

With the continuous development of the modern social economy, rubber has been widely used in our daily life. Tire and road wear particles (TRWPs) are generated by friction between tires and the road surface during the processes of driving, acceleration, and braking. TRWPs can be divided into three main components according to their source: tire tread, brake wear, and road wear. Due to urban runoff, TRWPs flow with rainwater into the aquatic environment and influence the surrounding aquatic organisms. As an emerging contaminant, TRWPs with the characteristics of small particles and strong toxicity have been given more attention recently. Here, we summarized the existing knowledge of the physical and chemical properties of TRWPs, the pathways of TRWPs into the water body, and the exposure routes of TRWPs. Furthermore, we introduced the biological effects of TRWPs involved in size, concentration, and shape, as well as key toxic compounds involved in heavy metals, polycyclic aromatic hydrocarbons (PAHs), N-(1,3-dimethylbutyl)-N’-phenyl-p-phenylenediamine (6PPD), and benzothiazole on aquatic organisms, and attempted to find the relevant factors influencing the toxic effects of TRWPs. In the context of existing policies that ignore pollution from TRWPs emissions in the aquatic environment, we also proposed measures to mitigate the impact of TRWPs in the future, as well as an outlook for TRWPs research.

Microplastics (MPs) are a heterogeneous class of pollutants fouling aquatic environments and they are hazardous to aquatic organisms. This study investigated the size-dependent effects of polystyrene microspheres (PSMPs) on the swimming ability, metabolism, and oxidative stress of juvenile grass carp (Ctenopharyngodon idella). Test fish were exposed to four sizes of PSMPs (0.07, 0.5, 5, and 20-μm), and swimming ability was tested after different exposure times (2, 7, and 15 days). To measure the effect on swimming ability, critical swimming speed (U_crit) was determined, and to assess metabolic effects, oxygen consumption (MO₂), routine metabolic rate (RMR), maximum oxygen consumption (MMR), and excess post-exercise oxygen consumption (EPOC) were determined. To assess the effects on oxidative stress, the activities of two antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) were determined in the liver and gills of test fish. After exposure to 20 μm PSMPs, there was a significant drop in U_crit compared to the control group (P<0.05), with decreases of 22 % on Day 2 and Day 7, and 21 % on Day 15. The RMR and MMR increased significantly (P<0.05), the RMR by 23.9 % on Day 2 and the MMR by 17.2 % on Day 2 and on Day 15, 44.7 % and 20.0 % respectively. The EPOC decreased with exposure time, by 31 % (0.07-μm), 45 %-(0.5-μm), 49 % (5-μm), and 57 % (20-μm) after 15 days. Exposure to the larger PSMPs increased CAT and SOD activity more than the smaller PSMPs and the increases began with SOD activity in the gills. The larger PSMPs were consistently more harmful to juvenile grass carp than the smaller PSMPs. Our results clearly show that PSMPs have detrimental effects on juvenile grass carp and provide additional scientific evidence that environmental monitoring and regulation of microplastic pollution is necessary.

Nanoplastics (NPs) and microcystin-LR (MC-LR) are two common and harmful pollutants in water environments, especially at aquafarm where are full of plastic products and algae. It is of great significance to study the toxic effects and mechanisms of the NPs and/or MC-LR on fish at the early stage. In this study, the embryo and larvae of a filtering-feeding fish, Aristichthys nobilis, were used as the research objects. The results showed that the survival and hatching rates of the embryo were not significantly affected by the environmental concentration exposure of these two pollutants. Scanning electron microscopy (SEM) observation displayed that NPs adhered to the surface of the embryo membrane. Transcriptomic and bioinformatic analyses revealed that the NPs exposure activated neuromuscular junction development and skeletal muscle fiber in larvae, and affected C5-Branched dibasic acid metabolism. The metabolic and biosynthetic processes of zeaxanthin, xanthophyll, tetraterpenoid, and carotenoid were suppressed after the MC-LR exposure, which was harmful to the retinol metabolism of fish. Excessive production of superoxide dismutase (SOD) was detected under the MC-LR exposure. The MC-LR and NPs coexposure triggered primary immunodeficiency and adaptive immune response, leading to the possibility of reduced fitness of A.nobilis during the development. Collectively, our results indicate that environmental concentration NPs and MC-LR coexposure could cause toxic damage and enhance sick risk in A.nobilis, providing new insights into the risk of NPs and MC-LR on filtering-feeding fish.

Polycyclic aromatic hydrocarbons (PAHs) are persistent organic pollutants ubiquitous in coastal ecosystems. The white shrimp Penaeus vannamei naturally inhabits in coastal areas and is cultivated in farms located nearby the oceans. PAHs can damage shrimp health, endanger natural populations, and lower shrimp aquaculture productivity. However, crustaceans have enzymes capable of metabolizing organic xenobiotics as PAHs and to neutralize reactive oxygen species (ROS) produced during xenobiotics metabolism. An important superfamily of xenobiotic-metabolizing and antioxidant enzymes are glutathione S-transferases (GSTs). In white shrimp, some GSTs are known, but they have been scarcely studied in response to PAHs. In this study we report the molecular cloning and bioinformatic characterization of two novel nucleotide sequences corresponding to cytosolic GSTs belonging the Delta and Theta classes (GSTD and GSTT). Both proteins genes have tissue-specific patterns of expression under normal conditions, that do not necessarily relate to GST activity and glutathione content. The expression of the GSTD and GSTT, GST activity and glutathione content was analyzed in juvenile P. vannamei exposed to two PAHs, naphthalene (NAP) and phenanthrene (PHE) in sub-lethal concentrations for 96 h. GSTD expression was up-regulated by the two PAHs, while GSTT expression was only induced by NAP. In contrast, GST activity towards CDNB was only up-regulated by PHE, suggesting differential effects of PAHs at gene and protein level. On the other hand, lower reduced glutathione content (GSH) caused by PAHs indicates its utilization for detoxification or antioxidant defenses. However, the GSH/GSSG did not change by PAHs treatment, indicating that shrimp can maintain redox balance during short-term sub-lethal exposure to NAP and PHE. Despite the variations in the responses to NAP and PHE, all these results suggest that the GSTD and GSTT genes could be useful biomarkers for PAH exposure in P. vannamei.

This study aimed to investigate the toxicity and endocrine disrupting potential of a complex mixture of polycyclic aromatic hydrocarbons (PAHs) in the estrogen pathway using hepatocytes of Nile tilapia Oreochromis niloticus, the hepatocytes were exposed to various concentrations of the PAH mixture, and multiple endpoints were evaluated to assess their effects on cell viability, gene expression, oxidative stress markers, and efflux activity. The results revealed that the PAH mixture had limited effects on hepatocyte metabolism and cell adhesion, as indicated by the non-significant changes observed in MTT metabolism, neutral red retention, and crystal violet staining. However, significant alterations were observed in the expression of genes related to the estrogen pathway. Specifically, vitellogenin (vtg) exhibited a substantial increase of approximately 120% compared to the control group. Similarly, estrogen receptor 2 (esr2) showed a significant upregulation of approximately 90%. In contrast, no significant differences were observed in the expression of estrogen receptor 1 (esr1) and the G protein-coupled estrogen receptor 1 (gper1). Furthermore, the PAH mixture elicited complex responses in oxidative stress markers. While reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels remained unchanged, the activity of catalase (Cat) was significantly reduced, whereas superoxide dismutase (Sod) activity, glutathione S-transferase (Gst) activity, and non-protein thiols levels were significantly elevated. In addition, the PAH mixture significantly influenced efflux activity, as evidenced by the increased efflux of rhodamine and calcein, indicating alterations in multixenobiotic resistance (MXR)-associated proteins. Overall, these findings, associated with bioinformatic analysis, highlight the potential of the PAH mixture to modulate the estrogen pathway and induce oxidative stress in O. niloticus hepatocytes. Understanding the mechanisms underlying these effects is crucial for assessing the ecological risks of PAH exposure and developing appropriate strategies to mitigate their adverse impacts on aquatic organisms.

The extensive use of herbicide metamifop (MET) in rice fields for weeds control will inevitably lead to its entering into water environments and threaten the aquatic organisms. Previous researches have demonstrated that sublethal exposure of MET significantly affected zebrafish development. Yet the long-term toxicological impacts of MET on aquatic life remains unknown. Herein, we investigated the potential effects of MET (5 and 50 μg/L) on zebrafish during an entire life cycle. Since the expression level of male sex differentiation-related gene dmrt1 and sex hormone synthesis-related gene cyp19a1b were significantly changed after 50 μg/L MET exposure for only 7 days, indicators related to sex differentiation and reproductive system were further investigated. Results showed that the transcript of dmrt1 was inhibited, estradiol content increased and testosterone content decreased in zebrafish of both sexes after MET exposure at 45, 60 and 120 dpf. Histopathological sections showed that the proportions of mature germ cells in the gonads of male and female zebrafish (120 dpf) were significantly decreased. Moreover, males had elevated vitellogenin content while females did not after MET exposure; MET induced feminization in zebrafish, with the proportion of females significantly increased by 19.6% while that of males significantly decreased by 13.2% at 120 dpf. These results suggested that MET interfered with the expression levels of gonad development related-genes, disrupted sex hormone balance, and affected sex differentiation and reproductive system of female and male zebrafish, implying it might have potential endocrine disrupting effects after long-term exposure.