Search

Residual antidepressants are of increasing concern worldwide, yet critical information on their long-term neurotoxic impacts on nontarget aquatic animals is lacking. Here, we investigated the long-term effects (from 0 to 150 days postfertilization) of the selective serotonin reuptake inhibitor citalopram (0.1-100 μg/L) on motor function, learning, and memory in zebrafish over two generations and explored the reversibility of the effect in F1 larvae. Unlike F0

Venlafaxine and citalopram have been commonly found in surface water and may disrupt fish reproduction, yet the long-term impact and the underlying mechanism are largely unknown. Here, zebrafish were exposed to 0.1-100 μg/L venlafaxine and citalopram for their entire life cycle from embryo to adult, respectively. After exposure for 180 days, the lowest observable effective concentration (LOEC) of venlafaxine and citalopram to significantly reduce the mean number of egg production in adults were 10 and 1 μg/L, respectively, whereas the fertilization rate displayed no significant changes. Further, we investigated the impacts of venlafaxine and citalopram in a reproductive context, including sperm quality and reproductive behaviour. In contrast, venlafaxine and citalopram exposure did not affect sperm quality but caused a reduction of reproductive behaviour (e.g., mating duration and mating interval) of adults exposed to 1-10 μg/L of the antidepressant. Transcriptomic profiling of the whole ovary revealed that lifecycle venlafaxine and citalopram exposure significantly affected the Na

Vortioxetine is increasing in popularity as a treatment for major depressive disorder and has been detected in wastewater effluent. However, information on the toxicity and environmental risk of vortioxetine in non-target organisms is scarce. Here, embryonic and juvenile zebrafish (Danio rerio) were used to assess the toxicity of vortioxetine (0, 1, 10, 30, 100, 300, and 1000 μg/L) after 120 h and 7 d of exposure, respectively. Vortioxetine induced significant toxicity during embryonic development, including effects on survival, hatching, basal heart rate, spontaneous tail coiling and developmental abnormalities, and inhibited larval locomotor activity at concentrations higher than 30 μg/L. Additionally, vortioxetine evoked anxiolytic-like behavior and caused histopathological changes to multiple organs (gills, heart, liver and intestine) in juvenile zebrafish. Significant increase in 5-HT content was observed in whole zebrafish larvae and juvenile brain tissues from animals treated with 1 or 100 μg/L vortioxetine. Notably, the lowest effective concentrations of vortioxetine for zebrafish were mainly in the range of 10-30 μg/L, which were slightly lower than the vortioxetine therapeutic concentrations. Risk quotients assuming conservative exposure assessments were above one in European countries indicating moderate risk for the behavioral endpoints assessed. We believe that these results highlight the adverse effects of vortioxetine on non-target organisms and that further investigations will be required to provide a higher confidence.

Fenvalerate is a broadly used type II pyrethroid with a potential toxic effect in fish. However, information on the immunotoxicity of fenvalerate in fish is scarce. Here, to discover the immunotoxicity of fenvalerate and its underlying mechanism in fish, adult Chinese rare minnow was exposed to fenvalerate at 0, 0.3, 1, and 3 μg/L for 28 days and then subjected to Pseudomonas fluorescens (P. fluorescens) challenge. Fenvalerate induced significant pathological changes, with disintegration of cell boundaries in the intestine, epithelial hyperplasia in gills, and vacuolation of hepatocytes at 3 μg/L treatment. Additionally, the pathological characteristics were more serious during P. fluorescens infection after fenvalerate exposure. A significant increase in neutrophil counts was observed after 3 μg/L fenvalerate exposure for 28 days (p0.05), whereas significantly increased monocyte and neutrophil counts and greatly decreased lymphocyte counts were detected at 24 h post-injection (hpi) with P. fluorescens (p0.05). Furthermore, obvious decreases in LYS, IgM, ALP, and C3 levels were detected in plasma after 3 μg/L fenvalerate exposure for 28 days, which was consistent with the results at 24 and 48 hpi. Notably, fish exposed to fenvalerate suppressed the transcription of TLR-NF-κB signaling pathway-relevant genes in response to P. fluorescens, accompanied by high mortalities and bacterial loads. Therefore, our results demonstrate that fenvalerate at environmentally relevant concentrations caused immunotoxicity in fish. This study highlights the importance of considering the combined effects of chemicals and pathogens to refine our ability to predict the effects of environmental contaminants on aquatic organisms.

Fish behaviors have great potential as models for the study of pharmacology, genetics, and neuroscience. Zebrafish (Danio rerio), Japanese medaka (Oryzias latipes) and Chinese rare minnow (Gobiocypris rarus) are popular freshwater animal models. However, their behavioral use in aquatic toxicology research is generally hampered by oversimplified behavioral tasks and the fact that they are not well-developed animal models for toxicology. Here, this study presented a comparative analysis of multiple behavioral traits (i.e., anxiety-like behavior, novel object recognition, social preferences, habituation to light-dark stimulus and noise stimulus, and spatial learning and memory). We found that only medaka (d-rR) presented a weak or no response to repeated light-dark stimulus and noise stimulus. In addition, no significant behavioral changes were observed for the three species of juvenile fish models after 7 days of exposure to 0.01% v/v carrier solvents (i.e., ethanol, acetone, and DMSO). In contrast to zebrafish and Chinese rare minnow, medaka showed no significant changes in spatial memory after subacute exposure to 1 mg/L imidacloprid or 2.5 μg/L chlorpyrifos (cpf); instead, a hyperactivity response in the open field test and reduced social time were induced by cpf and imidacloprid, respectively. Our results suggest that: (1) behavioral effects are negligible when using

To reveal the adverse effects of organophosphorus flame retardants (OPFRs) on aquatic organisms at the epigenetic level, male Chinese rare minnows were exposed to 0.24 mg/L tris(2‑butoxyethyl) phosphate (TBOEP), 0.04 mg/L tris(1,3‑dichloro‑2‑propyl) phosphate (TDCIPP), or 0.012 mg/L triphenyl phosphate (TPHP) for 14 days. The effects of sub-acute OPFR exposure on liver miRNA and the 3' isomiR expression profiles of Chinese rare minnows were investigated. Through small RNA sequencing and bioinformatics analysis, a total of 32, 84, and 19 differentially expressed miRNAs were detected for TBOEP, TDCIPP, and TPHP exposure, respectively (p 0.05). Target prediction of the differentially expressed miRNAs and pathway enrichment analysis indicated that predicted altered mRNAs for all three OPFRs were associated with metabolic pathways, whereas base excision repair was only predicted to be perturbed by the TPHP treatment. In addition, 3' isomiR-Us were unexpectedly abundant in all groups (e.g., miR-143), and TDCIPP strongly increased the ratio of 3' isomiR-U expression. Finally, histological examination and metabolic enzyme activity analyses werein agreement with the predicted metabolic pathways. As such, our study indicates that the investigation of epigenetics changes in miRNA gene transcription is a considerable method for the assessment of aquatic toxicity.

Clozapine (CLZ) is a neuroactive pharmaceutical that is frequently detected in aquatic environments. Although the cardiotoxicity, developmental toxicity, and neurotoxicity of CLZ in aquatic non-target organisms have been reported, its lipotoxicity and underlying mechanism are unknown. Therefore, in this study, 2-month-old Chinese rare minnows were exposed to 0, 0.1, 1, and 10 μg/L CLZ for 90 days. Overt dyslipidemia was observed after CLZ exposure, whereas the body weights of females significantly increased after CLZ exposure (p 0.05). In addition, obvious hepatocyte vacuolization and hepatic lipid droplet accumulation were observed at all treatment groups (p 0.05). The activities of sterol regulatory element binding proteins 1 (SREBP1) and fatty acid synthase (FAS) were significantly upregulated at the 1 and 10 μg/L CLZ treatment groups (p 0.05). Moreover, evident cell boundary disintegration of the intestinal villi and increasing mucus secretion were observed at all treatment groups (p 0.05). Furthermore, the diversity of the gut microbiota increased, whereas the relative abundances of Proteobacteria, Firmicutes and Bacteroidetes significantly increased after CLZ exposure (p 0.05). Furthermore, significantly increased bacterial secondary bile acid biosynthesis activity in Chinese rare minnows was observed after 1 μg/L CLZ exposure (p 0.05). Therefore, our findings confirmed that CLZ induced lipotoxicity by stimulating SREBP1 and affecting the bacterial secondary bile acid biosynthesis activity in Chinese rare minnows.

Carbamazepine (CBZ), an anticonvulsant and mood stabilizer, is ubiquitous distributed in aquatic environment. Though the toxicity and endocrine disrupting effect of CBZ on non-target organisms have been studied, its lipotoxity are scarcely known. To assess the lipotoxicity of CBZ, 2-month-old Chinese rare minnow were exposed to 0, 1, 10, and 100 μg/L CBZ for 90 d. Obvious dyslipidemia was observed after 30 d and 90 d exposure, whereas overt hyperlipidemia was observed in males at 100 μg/L treatments. Severe lipid droplet accumulation in livers was observed at 10 and 100 μg/L treatments for 30 d and in females, whereas those was observed at all treatments in males. In addition, serious mitochondria damage was observed in males at 100 μg/L treatments. After 90 d exposure, the enzyme activities of FAS and ACCα were significantly increased at 10 and 100 μg/L treatments, whereas HMGCR were markedly increased at 100 μg/L treatments (p

Bifenthrin (BF) is an insecticide that is commonly used to control agricultural and domestic pests and is widespread in aquatic environments. Although previous studies have found that BF is toxic to aquatic organisms, such a comprehensive study of the mechanism of toxic effects in bivalves is not common. In this study, to assess the toxic effects of BF on bivalves, adult Corbicula fluminea (C. fluminea) were exposed to 0, 1, 5, and 25 μg/L BF for 15 days. Transcriptome analysis revealed that BF exposure significantly altered the expression of genes involved in detoxification, antioxidation, and metabolism. Moreover, the ROS content and GST activity at 25 μg/L treatments were significantly increased (p 0.05), and significant increases of MDA concentration and CAT activity were observed at 5 and 25 μg/L treatments (p 0.05). However, AChE activity was markedly inhibited at 25 μg/L treatments (p 0.05). In addition, vacuolation in the digestive tubules and the hemolytic infiltration of connective tissue were observed at all treatments, and the degeneration of the digestive tubule was observed at 5 and 25 μg/L treatments. In the behavioural assay, the siphoning behaviour of C. fluminea was significantly inhibited at 25 μg/L treatments (p 0.05), whereas no significant change in burrowing behaviour was observed. Our findings suggested that BF exposure caused changes in detoxification, antioxidation, and metabolism pathways, biomarker activity or concentrations and histopathological characteristics, resulting in changes in behaviour. Therefore, our findings provide a basis for further evaluation of the toxicity of pyrethroid insecticides in bivalves.

The presence of pharmaceutical residues in aquatic ecosystems is a worldwide problem that may pose serious threats and challenges to the environment, especially to the safety of aquatic biota. In the present study, we investigated the effects of 14 environmentally relevant pharmaceutical compounds on individual and collective-related behaviours in juvenile zebrafish (Danio rerio) for 21 days. The tested concentrations of the compounds spanned three orders of magnitude. This study also compared the potential risks of these compounds in Chinese surface waters based on the data on their toxic effects or only on behavioural effects. In the case of individual behaviours, most antidepressants, but not anti-inflammatory agents or blood lipid-lowering agents, decreased fish locomotor activity (LMA) and individual social activity (IDS); however, all three classes of compounds induced significant disruptions in the light/dark transition locomotor response (LMR-L/D) performance, even at lower treatment levels (0.1–1 μg/L). Furthermore, collective behaviour (CLB) analysis suggested that most of the compounds significantly altered the group sociability of fish and frequently occurred at environmentally relevant concentrations. Finally, a risk assessment suggested that the presence of ibuprofen, fluoxetine, and venlafaxine in the surface waters of China poses a relatively high risk to fish, regardless of the risk ranking based on the data of the toxic or behavioural effects.

To assess the toxic effects of 3-(4-Methylbenzylidene) camphor (4-MBC) at environmentally relevant concentrations on the reproduction and development of Japanese medaka (Oryzias latipes), adult paired medaka (F0) were exposed to 5, 50, and 500 μg/L 4-MBC for 28 d in the current study. The fecundity and fertility were significantly decreased at 500 μg/L 4-MBC (p

The growing use of octocrylene (OC) in sunscreens has posed a great threat to aquatic organisms. In the present study, to assess its reproductive toxicity and mechanism, paired Japanese medaka (Oryzias latipes) (F0) were exposed to OC at nominal concentrations of 5, 50, and 500 μg/L for 28 d. Significant increases were observed in the gonadosomatic index (GSI) and hepatosomatic index (HSI) of F0 medaka at 500 μg/L OC (p

Organophosphate flame retardants (OPFRs) are widespread in the aquatic environment, but the effects of these chemicals on reproductive toxicity are far from clear. In this study, sperm quality in adult male Chinese rare minnows after exposure to tris-(2-butoxyethyl) phosphate (TBOEP), tris-(1,3-dichloro-2-propyl) phosphate (TDCIPP), and triphenyl phosphate (TPHP) was investigated. No obvious change in sperm concentration and vitality was observed after treatments, whereas significant changes in sperm velocity and morphology were found following all treatments (P 0.05). Moreover, OPFR exposure significantly increased the apoptosis ratios in testis cells. Analysis of the transcriptomic data revealed that Na

In the current study, to investigate the effect of imidacloprid on benthic bivalves, adult Asian clams (Corbicula fluminea) were exposed to 0, 20, 200, and 2000 μg/L imidacloprid for 30 d. Imidacloprid significantly inhibited the siphoning and burrowing behaviour (p 0.05) of the clams. Significant histopathological changes were associated with degeneration of the cilium, the contraction and adhesion of the lymphocyte, and the swelling of epithelium cells in gills, and there was notable degeneration in the digestive tubules, haemolytic infiltration in the connective tissue and epithelial cell necrosis in the digestive glands in the 2000 μg/L treatment group. The activity of AChE in the digestive glands was significantly inhibited at all treatment levels, whereas this inhibition was observed in gills only in the 2000 μg/L treatment (p 0.05). Additionally, indicators of the antioxidant system (e.g., SOD, CAT, and GST activity) and MDA content were significantly increased in the gills and digestive glands with all treatments (p 0.05). Moreover, the mRNA expression levels of Hsp genes (hsp 22, hsp 40, hsp 60, hsp 70, hsp 90) and multixenobiotic resistance (MXR) system-related genes (abcb1, abcc1) were significantly downregulated (p 0.05). Therefore, our results suggest that imidacloprid changes the oxidative stress, cellular detoxification, and MXR system of C. fluminea. Our findings provide new insights into the effects of neonicotinoids on benthic bivalves such as C. fluminea.

The neurotoxicity of triphenyl phosphate (TPHP) in exposed humans and laboratory animals is under debate. The rapid crossing of the blood-brain barrier (BBB) and high distribution of TPHP in fish brains have raised widespread concerns about potential neurotoxicity. Adult male Chinese rare minnows ( Gobiocypris rarus) were used as a model and exposed to 0, 20, or 100 μg/L TPHP for 28 days. We evaluated the BBB permeability, neuroinflammatory response, cell proliferation and apoptosis, synaptic plasticity and synapse loss in fish brains via the learning/memory performance of fish following 28 days of TPHP exposure. TPHP significantly increased the BBB permeability, activated the neuroinflammatory response, and decreased the tight junction-related mRNA levels of claudin-5α and occludin in the fish brain. In addition, cell proliferation was inhibited by treatment with 100 μg/L TPHP, but no significant apoptosis was observed in the brain. Fish exposed to 100 μg/L TPHP exhibited significantly decreased dendritic arborization in pyramidal neurons in the cerebellum (Ce), and the maze test indicated impaired learning/memory performance. Taken together, these findings provide scientific evidence that TPHP is neurotoxic to fish and further suggest that TPHP may not be a safe alternative for aquatic organisms.

In the present study, to discover new biomarker of Asian freshwater clam (Corbicula fluminea) to assess impact of environmental pollutions, cholecystokinin (CCK), conopressin, and Neuropeptide FF (FFamide) in C. fluminea were selected as potent biomarkers. Therefore, their full-length cDNAs were cloned and characterized to investigate the molecular characteristics and expression patterns of neuropeptides in C. fluminea. According to the sequence analysis, CCK, conopressin, and FFamide encoded proteins of 173, 152, and 90 amino acids, respectively. Moreover, the multiple sequence alignment revealed that the bioactive regions of these neuropeptides were well conserved among different invertebrates. In addition, under basal conditions, CCK, conopressin and FFamide mRNA were mainly expressed in the visceral mass, whereas the FFamide mRNA was rarely detected in the foot and mantle. Exposure to 20 and 200 μg/L Tris (2-butoxyethyl) phosphate (TBOEP) and tri-butyl-phosphate (TBP) exposure significantly up-regulated the expression of the CCK and FFamide mRNAs in the visceral mass (p 0.05), whereas no significant changes in conopressin mRNA levels were observed in response to any treatment. Therefore, CCK and FFamide of C. fluminea neuropeptides are feasible new biomarkers for screening and assessing responses to organophosphate chemicals.

Phenanthrene (Phe) is one of the most abundant low-molecular-weight polycyclic aromatic hydrocarbons (PAHs). Widespread human and aquatic organism exposure to Phe has been reported, but the toxic effects of Phe and potential mechanisms are unclear. We focused on the chronic hepatotoxicity of Phe in adult Chinese rare minnows (Gobiocypris rarus) and the underlying mechanisms. The chronic effects of exposing Chinese rare minnows to 8.9, 82.3, or 510.0 μg/L Phe for 30 days were examined by histopathological observation, TUNEL assays, caspase activity assays, and gene expression profiles. The liver lesion frequency and hepatocyte apoptosis were increased in Phe-exposed groups. Caspase 9 and caspase 3 enzyme activity in liver tissues was markedly increased. The expression of miR-17/92 cluster members was significantly increased in the 82.3 and 510.0 μg/L groups. Moreover, the response of primary hepatocytes indicated a significant decrease in the mitochondrial membrane potential (MMP) after a 48 h exposure to Phe. Interestingly, miR-18a was significantly decreased in primary hepatocytes in all treatments. Moreover, molecular docking indicated that Phe might have the same binding domain as pri-miR-18a, forming pi-pi and pi-σ interactions with heterogeneous nuclear ribonucleoprotein (hnRNP) A1. Given the above, Phe caused liver lesions and induced hepatocyte apoptosis through the intrinsic apoptosis pathway, and the interaction of Phe with hnRNP A1 contributes to the suppression of miR-18a expression and hepatocyte apoptosis.

In this study, the cDNA fragments of cytokines (il-8) and toll-like receptor (TLR) pathway signaling molecules (myd88, irak-1, irf5, and irf7) in the Chinese rare minnow were cloned and exhibited a high amino-acid sequence identity compared to other cyprinid fish orthologs. The mRNA expressions of these genes in the different tissues (liver, brain, spleen, kidney, and skin) were observed. The highest expression levels of myd88, irak-1, and irf5 were detected in the spleen, whereas il-8 and irf7 were detected in the kidney and liver respectively. The mRNA expression of irak-1, irf5, and irf7 in the liver from 0.1 μg/L and 0.5 μg/L CPF treatments were significantly increased on day 7 (p < 0.05), whereas the levels of only irak-1 and irf7 were markedly increased on day 28 (p < 0.05). Moreover, the mRNA expression of il-8 in the spleen following 0.5 μg/L CPF treatments was significantly decreased on day 7 (p < 0.05), whereas significantly decrease were observed in the levels of irf7 in the spleen at 2.5 μg/L CPF on days 7 and 28 (p < 0.05). The 0.1 μg/L and 0.5 μg/L of CPF significantly induced the levels of irak-1 and myd88 in the spleen after 28 d exposure (p < 0.05). Therefore, the high induction of cytokines and TLR pathway signaling molecules demonstrated that Chinese rare minnow was immune-compromised exposed to CPF. Moreover, our finding indicated that these immune-related genes could be feasible to screen for substances hazardous to the immune system of fish.

Adverse impacts of immunity in terrestrial non-target organisms exposed to neonicotinoid insecticides have been reported, but the causal link between insecticide exposure and possible immune alterations in fish remains limited. In the present study, the potential genotoxicity and immunotoxicity of three neonicotinoids (imidacloprid, nitenpyram, and dinotefuran) were assessed in Chinese rare minnows by using a 60-day chronic toxicity test. The hematological and biochemical parameters of juvenile Chinese rare minnows and changes in the transcription of six inflammation-related genes were determined after exposure to neonicotinoids at 0.1, 0.5, or 2.0 mg/L. A clear difference in the frequency of erythrocytes with micronuclei (MN) was observed after treatment with 2.0 mg/L imidacloprid (p .05). Additionally, exposure to 0.5 or 2.0 mg/L imidacloprid significantly increased the binucleated (BN) erythrocytes and those with notched nuclei (NT) (p .05). A serum protein electrophoresis (SPE) assay showed significant alterations in the serum protein in all treatments (p .05), and further analysis indicated decreases in immunoglobulin (Ig) in treatments with 0.5 or 2.0 mg/L imidacloprid or dinotefuran or with 0.1 mg/L nitenpyram (p .05). Moreover, a biochemical assay confirmed that immunoglobulin M (IgM) levels were indeed significantly decreased upon treatment with imidacloprid or dinotefuran at 0.5 or 2.0 mg/L (p .05). In addition, the transcriptional levels of the inflammatory cytokines IL-6, INF-α, TNF-α, and IL-1β were markedly down-regulated after all imidacloprid treatments (p .05), whereas the expression levels of only TNF-α and IL-1β were significantly down-regulated following the 0.5 and 2.0 mg/L dinotefuran treatments (p .05). Taken together, our results clearly demonstrate that imidacloprid, rather than nitenpyram and dinotefuran, can induce genotoxicity. The responsiveness of these immune indicators provides new insight into and evidence of the adverse effects of neonicotinoids on aquatic non-target organisms.

To examine the effects of BaP on tissue apoptosis, laboratory studies were conducted using juvenile Chinese rare minnows (Gobiocypris rarus) exposed to 1, 5, 20, and 80 μg/L of BaP for 28 days. The post-treatment pathological findings in the liver were associated with hepatocyte swelling, karyopyknosis, and karyorrhexis. Moreover, an increase in the goblet cells in the intestine, epithelial hyperplasia of the gills and fusion of gill lamellae were observed. Significant increases in hepatocyte apoptosis using the TUNEL stain were observed in the liver tissue but not in the intestine and gills. In addition, BaP exposure significantly up-regulated the mRNA levels of cyp1a1, p53, bax, bcl-2, and caspase-9 in the liver following the 5, 20, and 80 μg/L treatments, whereas the apaf-1 was significantly down-regulated following all treatments. Moreover, the activities of caspase 3 and caspase 8 were markedly elevated, whereas the protein expression levels of Apaf-1 were down-regulated following the 20 and 80 μg/L treatments. Taken together, our results suggested that BaP strongly induces tissue-specific apoptosis in vivo, leading to significant pathological changes. The responsiveness of apoptotic-related genes demonstrates that BaP induced apoptosis in the liver may be through a mitochondria-independent pathway.

Background MicroRNAs (miRNAs), which comprise a large family of endogenous small non-coding RNA molecules, play important roles in the regulation of gene expression in various biological processes. The Chinese rare minnow (Gobiocypris rarus) is a Chinese native fish species and is used extensively as an experimental fish in China; however, relevant biological data, especially miRNA transcriptome data, have not been well documented. To discover conserved and potential novel miRNAs in Chinese rare minnows, a pool of equal amounts of RNA obtained from 6 different adult rare minnow tissues (brain, eye, gill, liver, muscle and heart) was sequenced using illumina deep sequencing technology. Results In the present study, 26,930,553 raw reads, representing 2,118,439 unique high-quality reads, were obtained from the pooled small RNA library. Using bioinformatics analysis, 352 conserved and 112 novel Chinese rare minnow miRNAs were first discovered and characterized in this study. Moreover, we found extensive sequence variations (isomiRs) in rare minnow miRNAs, including internal miRNA isomiRs and terminal isomiRs at both the 5′ and 3′ ends and nucleotide variants. Six conserved and 4 novel miRNAs were selected and validated in 6 different adult rare minnow tissues using quantitative real-time PCR (qPCR). The results showed that miR-30a, miR-30b, and Novel-37 are ubiquitously expressed in a variety of tissues. miR-16a, miR-9, miR-125b, miR-34a, and Novel-69 were predominantly expressed in the brain. Novel-115 and Novel-7 were highly expressed in gills, but were relatively weakly expressed in other tissues. These results provided the expression patterns of miRNA genes in Chinese rare minnow. Finally, based on bioinformatics predictions, we mainly found that Novel-94 and Novel-1b-5p were simultaneously targeted to the 3′UTR of Dmrt1, which controls sex determination and/or sexual differentiation in a variety of metazoans at different sites. Novel-29b targeted the 3′UTR of Foxl2, which is involved in the maintenance of ovarian function and the transcriptional regulation of gonadal differentiation-related genes. Novel-62 and Novel-53 targeted the 3′UTR of ERbeta1 and ERbeta2 (which regulate the transcription of target genes), respectively. Conclusions Rare minnow is a widely used model for assessing the risk of environmental pollution in China. Identifying and characterizing rare minnow miRNA genes is necessary to discover the biological function of miRNAs and to screen for new molecule biomarkers to assess the risk of environmental pollution in the future. Electronic supplementary material The online version of this article (doi:10.1186/s12864-016-2606-5) contains supplementary material, which is available to authorized users.