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The trophic interactions between consumers and resources play a vital role in the stability of communities. In river systems, fragmentation of natural habitats and environmental changes alters the energy basis and community composition, consequently leading to variations in the community's trophic structure and niche space. However, our understanding of how the trophic structure responds to environmental changes is still very limited. Here, based on stable isotope data, we explored and compared trophic positions (TPs), community‐wide trophic metrics, and isotope niche space of fish communities in three reaches with different hydrogeomorphic conditions along a highly regulated subtropical river over three seasons. The community trophic structure and niche space showed notable spatiotemporal variations. Overall, the downstream reach had lower TPs, trophic diversity but higher trophic redundancy. The middle reach occupied a wider isotope niche space than other reaches, with the largest niche size during autumn. Furthermore, the niche overlap was relatively high in winter between reaches and in the downstream between seasons. The results implied a homogenization of feeding functional groups and energy flow pathways of species in the downstream community associated with the change of energy source and stability of hydrological conditions. The relationship between trophic structure and environmental factors suggested that the dam‐induced alteration in hydrological‐related aspects may drive the changes in the functional group composition, together with changes in energy basis, resulting in differences in the trophic structure of the community. The results of the present study deepen our understanding of how ecosystem functions respond to disturbance, thus contributing to improved ability to conserve river ecosystems. [ABSTRACT FROM AUTHOR]

The river discontinuity caused by damming can modify both the availability of production sources and the energy flow in riverine food webs. We hypothesized the carbon source support food web would vary among the reaches in response to changing in hydrogeomorphic conditions, and this variability further caused food web structure changes. To test our hypothesis, three different river reaches in the lower Jinsha River, China, were selected and the stable isotope ratios of basal sources and dominant consumers were analyzed in three seasons 2015. The relative importance of basal sources showed temporal and spatial difference to varying degrees. Seston were the most important carbon sources in supporting all consumers and the contributions increased from upstream to downstream. Riparian C3 plants played an important supplementary role in both reaches above the dam or only in the high flow period. Dam-induced flow alteration changed the trophic basis and the composition of food webs, resulting in a difference in the food web structures, and widening but with lowest complexity food web occurred in the downstream reach. The results further confirm that the differences in the hydrogeomorphologic conditions caused by dam construction can exert potential influence on riverine food web structures. [ABSTRACT FROM AUTHOR]

• o,p' -DDT and p,p′- DDE cause developmental toxicity in zebrafish larvae. • o,p' -DDT exposure significantly increased whole-body thyroid hormone levels. • p,p′- DDE exposure significantly decreased whole-body thyroid hormone levels. • The gene expression patterns of HPT axis were changed after exposure to either o,p' -DDT or p,p′ -DDE. 1,1-Trichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl) ethane (o,p' -DDT) and 1,1-dichloro-2,2-bis (p-chlorophenyl)-ethylene (p,p′- DDE) cause thyroid disruption, but the underlying mechanisms of these disturbances in fish remain unclear. To explore the potential mechanisms of thyroid dysfunction caused by o,p' -DDT and p,p′- DDE, thyroid hormone and gene expression levels in the hypothalamic-pituitary-thyroid (HPT) axis were measured, and the developmental toxicity were recorded in zebrafish larvae. Zebrafish embryos/larvae were exposed to o,p' -DDT (0, 0.28, 2.8, and 28 nM; or 0, 0.1, 1, and 10 μg/L) and p,p′- DDE (0, 1.57, 15.7, and 157 nM; or 0, 0.5, 5, and 50 μg/L) for 7 days. The genes related to thyroid hormone synthesis (crh , tshβ , tg , nis and tpo) and thyroid development (nkx2.1 and pax8) were up-regulated in both the o,p' -DDT and p,p′- DDE exposure groups. Zebrafish embryos/larvae exposed to o,p' -DDT showed significantly increased total whole-body T4 and T3 levels, with the expression of ugt1ab and dio3 being significantly down-regulated. However, the p,p′- DDE exposure groups showed significantly lowered whole-body total T4 and T3 levels, which were associated with up-regulation and down-regulation expression of the expression of dio2 and ugt1ab , respectively. Interestingly, the ratio of T3 to T4 was significantly decreased in the o,p' -DDT (28 nM) and p,p′- DDE (157 nM) exposure groups, suggesting an impairment of thyroid function. In addition, reduced survival rates and body lengths and increased malformation rates were recorded after treatment with either o,p' -DDT or p,p′- DDE. In summary, our study indicates that the disruption of thyroid states was different in response to o,p' -DDT and p,p′ -DDE exposure in zebrafish larvae. [ABSTRACT FROM AUTHOR]

• TPT exposure caused thyroid disruption in zebrafish. • TPT exposure changed the liver metabolizing enzymes in zebrafish. • Thyroid disruption and detoxifying enzyme capacities changed were sex-specific in zebrafish. Although organotin compounds are known to disturb thyroid signaling and antioxidant defense system, the sex-differences underlying these effects of triphenyltin chloride (TPT) in fish remain unclear. To understand these differences, adult zebrafish (Danio rerio) were exposed to different concentrations of TPT (0, 10, 100, or 1000 ng/L) for 28 days. Female zebrafish exposed to TPT showed significantly increased thyroxine (T4) content and decrease triiodothyronine (T3) content, possibly due to downregulation of deiodinase (dio2) and uridine diphosphate glucuronosyl transferase (ugt1ab). However, decreased T4 and T3 contents in male zebrafish accompanied with upregulation of dio1 , dio2 and ugt1ab. TPT exposure can lead to sex-specific thyroid disruption in adult zebrafish via alterations the Hypothalamus-pituitary-thyroid-liver axis. In addition, the gene expression levels of metabolizing enzymes, such as cyp1b , cyp1c , gpx1a , or sult1st1 were also to vary in a sex-dependent manner in adult zebrafish liver. Downregulation of cyp19a and cyp19b and decreased 17β -estradiol (E2) contents were detected in both female and male zebrafish. Therefore, a sex-specific of thyroid disruption response after TPT exposure was observed in adult zebrafish, possibly due to inherent in female or males detoxifying enzyme capacities. [ABSTRACT FROM AUTHOR]

Although polybrominated diphenyl ethers (PBDEs) are known to disturb thyroid hormone signaling, the mechanisms underlying the effects of 2,2′,4,4′5 - pentain polybrominated diphenyl ethers (BDE-99) in fish remain unclear. In order to reveal these mechanisms, adult zebrafish (Danio rerio) were exposed to different concentrations of BDE-99 (0, 0.5, 5, or 50 μg/L) for 28 days and spawned by mating naturally in clean water (without BDE-99). Females exposed to BDE-99 showed significantly lowered thyroxine (T4) levels. Expression of transthyretin (ttr) and uridine diphosphate glucuronosyl transferase (ugt1ab) were down-regulated and up-regulated, respectively. Triiodothyronine (T3) levels in the 0.5 μg/L BDE-99 exposure group was significantly increased. Males showed significantly increased T3 levels, and lowered T4 levels, which were associated with up-regulated and down-regulated expression of deiodinase 2 (deio2) and ugt1ab , respectively. Exposure of adult zebrafish to BDE-99 lead to significantly increased T4 in the 0.5 μg/L BDE-99 exposure group, but in the 50 μg/L BDE-99 exposure group there was significantly reduced T4 in F1 larvae and altered mRNA transcription in the hypothalamic-pituitary-thyroid-liver (HPTL) axis. The offspring also showed reduced survival rates, and body length and elevated malformation rates. This study is the first in zebrafish to show that parental zebrafish exposure to BDE-99 can lead to developmental toxicity and thyroid disruption in the offspring. • Chronic exposure to BDE-99 in a zebrafish model was tested. • BDE-99 exposure causes thyroid endocrine disruption in the adult zebrafish. • BDE-99 exposure causes thyroid endocrine disruption and developmental toxicity in offspring larvae. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs) are well-known contaminants with widespread distribution in environment and food. Phenanthrene is one of the most abundant PAHs in food and aquatic environment and generates reproductive and developmental toxicity in zebrafish. Nonetheless, whether phenanthrene caused sex-specific thyroid disruption in adult zebrafish is unclear. To determine this, adult zebrafish (male and female) were treated with phenanthrene (0, 0.85, 8.5, and 85 μg/L) for 60 days. After the treatment period, we assessed the concentrations of thyroid hormones (THs) and expression levels of genes in the hypothalamic-pituitary-thyroid (HPT) axis. The results showed that phenanthrene exposure can lead to thyroid disruption in both male and female zebrafish. Exposure to phenanthrene dramatically reduced the levels of L-thyroxine (T4) and L-triiodothyronine (T3) in both male and female zebrafish, with a similar trend in both. However, the genes expression profiles of hypothalamic-pituitary-thyroid (HPT) axis were sex-specific. In all, the present study demonstrated that phenanthrene exposure could result in sex-specific thyroid disruption in adult zebrafish. [Display omitted] • Phenanthrene exposure caused thyroid disruption in both male and female zebrafish. • Phenanthrene exposure deduced thyroid hormones regardless of gender. • The genes expression profiles of HPT axis were sex-specific after phenanthrene exposure. [ABSTRACT FROM AUTHOR]

• Phenanthrene accumulated rapidly and then quickly decreased in zebrafish embryos/larvae. • Phenanthrene caused thyroid disruption via the HPT axis. • Phenanthrene caused growth inhibition via the GH/IGF-1 axis. Phenanthrene induces reproductive and developmental toxicity in fish, but whether it can disrupt the thyroid hormone balance and inhibit growth had not been determined to date. In this study, zebrafish embryos were exposed to phenanthrene (0, 0.1, 1, 10 and 100 μg/L) for 7 days. The results of this experiment demonstrated that phenanthrene induced thyroid disruption and growth inhibition in zebrafish larvae. Phenanthrene significantly decreased the concentration of l -thyroxine (T4) but increased that of 3,5,3′- l -triiodothyronine (T3). The expression of genes related to the hypothalamic-pituitary-thyroid (HPT) axis was altered in zebrafish larvae exposed to phenanthrene. Moreover, phenanthrene exposure significantly increased the malformation rate and significantly reduced the survival rate and the body length of zebrafish larvae. Furthermore, phenanthrene significantly decreased the concentrations of growth hormone (GH) and insulin-like growth factor-1 (IGF-1). Changes observed in gene expression patterns further support the hypothesis that these effects may be related to alterations along the GH/IGF-1 axis. In conclusion, our study indicated that exposure to phenanthrene at concentrations as low as 0.1 μg/L resulted in thyroid disruption and growth inhibition in zebrafish larvae. Therefore, the estimation of phenanthrene levels in the aquatic environment needs to be revisited. [ABSTRACT FROM AUTHOR]

In recent years, the adverse effects of cadmium (Cd2+) on aquatic systems have attracted much attention because Cd2+ can induce endocrine disorders and toxicity in aquatic organisms at low levels. However, its effects on the thyroid system in native fish in Lhasa are still unclear. In the present study, Schizopygopsis younghusbandi larvae were exposed to Cd2+ (0.25, 2.5, 25 or 250 μg/L) for 7 or 14 days to determine its toxic effects on thyroid function. The results showed that whole-body total T4 and T3 levels were significantly decreased, which was accompanied by the significant upregulation of the expression of the dio1 and dio2 genes after exposure to Cd2+ for 7 or 14 days. Genes related to thyroid hormone synthesis (crh and tshβ) were upregulated after both 7 and 14 days of Cd2+ exposure, possibly due to the negative feedback regulation of the hypothalamic-pituitary-thyroid (HPT) axis caused by a decrease in thyroid hormone. In addition, survival rates and body lengths were reduced after treatment with Cd2+. This suggests that Cd2+ caused developmental toxicity in Schizopygopsis younghusbandi larvae. An integrated assessment of biomarker response (IBR) showed that there were dose-dependent and time-dependent effects of Cd2+ exposure on Schizopygopsis younghusbandi larvae. Schizopygopsis younghusbandi larvae were sensitive to Cd2+, which caused adverse effects at a concentration as low as 2.5 μg/L. In summary, the results indicated that Cd2+ causes thyroid disruption and developmental toxicity in Schizopygopsis younghusbandi larvae and that wild Schizopygopsis younghusbandi larvae living in the Lhasa River are at potential ecological risk. Unlabelled Image • Cd2+ exposure causes developmental toxicity in Schizopygopsis younghusbandi larvae. • Cd2+ exposure causes thyroid disruption in Schizopygopsis younghusbandi larvae. • Schizopygopsis younghusbandi larvae face ecological risks in the Lhasa River. [ABSTRACT FROM AUTHOR]

The adverse effects of triphenyltin (TPT) on aquatic systems have attracted much attention because TPT is widely used and prevalent in aquatic environments. Here, zebrafish embryos/larvae were exposed to TPT (0, 0.039, 0.39, and 3.9 nM; 0, 15, 150 and 1500 ng/L) for 7 or 14 days to determine its toxic effects on the hypothalamic–pituitary–thyroid (HPT) axis. The results showed that whole-body total T4 and T3 levels were significantly decreased, which was accompanied by the significant upregulation of the expression of the dio1 , dio2 and ugt1ab genes after exposure to TPT for 7 and 14 days. Genes related to thyroid hormone synthesis (crh , tshβ , nis, tpo and tg) were upregulated at both 7 and 14 days after TPT exposure. This might have been due to the positive feedback regulation of the HPT axis, which is caused by a decrease in thyroid hormone in the whole body in zebrafish. In addition, the survival rates and body lengths were reduced after treatment with TPT for 7 and 14 days. This indicated that TPT caused adverse effect on the development of zebrafish embryos/larvae. In summary, the results suggested that TPT caused thyroid disruption and developmental toxicity in zebrafish larvae. Unlabelled Image • TPT exposure caused developmental toxicity in zebrafish larvae. • The gene expression patterns of the HPT axis were changed after TPT exposure. • TPT significantly decreased whole-body thyroid hormone levels. • TPT at environmental dose caused thyroid disruption in zebrafish larvae. [ABSTRACT FROM AUTHOR]

• 4 locomotor groups and 4 trophic groups were classified in the Anning River. • Environmental variables, taxonomic and functional groups exhibited significant changes with respect to the DFH. • Spatial changes in taxonomic and functional groups along the river were primarily due to turnover processes. • The influence of landscape features on functional organizations was more significant compared to local habitat variables. To investigate the longitudinal gradient patterns and the factors influencing fish taxonomic and functional groups, a survey involving 28 sampling sites was conducted in the Anning River in November 2020 and April 2021. A total of 60 fish species were collected, and these species were classified into 4 locomotor groups and 4 trophic groups, resulting in 11 combined functional groups based on locomotor and trophic characteristics. The results of two-way cross similarity analysis (ANOSIM) revealed significant changes in both the fish taxonomic and functional groups along the longitudinal gradient, while no significant seasonal variation was observed in either group. Spatial changes in taxonomic and functional groups along the river were primarily due to turnover processes, as indicated by the similarity percentage analysis. Variance partitioning analysis demonstrated that local habitat conditions and land use/cover explained 37.56% and 41.33% of the spatial variation in taxonomic and functional organizations, respectively. Notably, the influence of landscape features on taxonomic organization was less significant than that of local habitat variables. Nevertheless, landscape conditions played a more important role than local environmental factors in explaining variations associated with functional organization. Our study helps in understanding the spatial patterns and formation mechanisms of taxonomic and functional groups driven by multiple-scale environmental factors in mountain rivers. In addition, our results showed that the response of functional groups to different scale environmental factors differ from taxonomic groups. [ABSTRACT FROM AUTHOR]

The length–weight relationships (LWRs) for 15 fish species from the Three Gorges Reservoir (TGR) were described in this paper. Specimens were collected using gill nets (mesh size: 6, 8, 10, 12 cm), cage net (mesh size: 1 cm), benthic fyke net (mesh size: 1 cm), hook longlines (80 m long, 3 barbless hooks per meter line) and electrofishing (power: 1,500 w; distance of electrodes: 1–2 m; water depth: 0.2–1.0 m; water area: 1–2 m2; catch by dip net [mesh size: 0.4 cm]) at four sections of the TGR, monthly in June–August and October–November in 2017 and 2018. The first LWR reference for Zacco acutipinnis (Bleeker, 1871), Discogobio brachyphysallidos Huang, 1989, Squalidus nitens (Günther, 1873), Leptobotia pellegrini Fang, 1936, Sinibotia reevesae (Chang, 1944), Pseudobagrus tenuifurcatus (Nichols, 1931), Pseudobagrus medianalis (Regan, 1904), Liobagrus marginatoides (Wu, 1930), Glyptothorax fokiensis (Rendahl, 1925), and Ctenogobius szechuanensis (Liu, 1940) and new maximum total length for 12 species are provided. [ABSTRACT FROM AUTHOR]