Ovarian development in the Chinese mitten crab (Eriocheir sinensis) enters a rapid development period after the reproductive molt. During this process, low-temperature stimulation seems to be a key initiating factor. To verify this, the current study simulated a nine-week long-term low-temperature experiment during the fattening stage in an indoor thermostatic water circulation system, including a high-temperature control group (30 degrees C), a medium-temperature group (25 degrees C) and low-temperature group (20 degrees C). Based on multi-omics sequencing and histological analysis, we found that chronic low-temperature exposure promotes ovarian development by upregulating the mRNA expression of crucial genes (e75/74, vg/vgr, 17 beta-estradiol, er alpha) and promoting the secretion of GIH, MF, and E2 hormones. This can be evidenced by the densely distributed yolk granules, significantly increased oocyte diameter, and GSI index. Interestingly, the significantly increased lipid droplet area and crude lipid level indicate that chronic cold stimulation can promote fat accumulation in the ovary. Significantly, the peroxisome proliferator-activated receptor (PPAR) signaling pathway and phospholipids, including phosphatidylcholine (PC) and phosphatidylethanolamine (PE), play important roles in this process. In addition, continuous cold exposure can significantly increase the levels of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) of hepatopancreas and ovarian tissue, and inhibit the synthesis of saturated fatty acids (SFAs) to promote the deposition of nutrients and flavor substances. In conclusion, our current data reveal a series of physiological responses to continuous cold exposure during fattening, providing valuable data support for the fattening strategy and quality improvement of Chinese mitten crabs.

Oxidative stress represents a critical threat to aquatic animal health and aquaculture productivity. Allicin, a natural plant extract, has not been systematically investigated for its antioxidant mechanisms in aquatic crustaceans. This study established in vitro and in vivo models of tert-butyl hydroperoxide (T-BHP)-induced oxidative stress in Chinese mitten crabs (Eriocheir sinensis) to evaluate the hepatoprotective effects of allicin. Integrating biochemical, transcriptomic, and ultrastructural analyses, we found that allicin significantly alleviated T-BHP-induced cytotoxicity and oxidative damage in vitro. Mechanistically, allicin up-regulated antioxidant genes including glutathione peroxidase (gpx) and thioredoxin reductase 1 (trxr1), and down-regulated pro-inflammatory cytokines such as interleukin-1 beta (il-1β), suggesting the concomitant activation of the Nrf2 signaling pathway and inhibition of the p38-MAPK/NF-κB pathway. Transcriptomics further indicated its role in restoring proteostasis and mitochondrial function. A 35-day feeding trial validated these findings in vivo; dietary supplementation with 300 mg·kg-1 allicin effectively reversed T-BHP-induced disturbances in antioxidant enzyme activities and immune-related gene expression. These consistent findings demonstrate that allicin alleviates hepatopancreatic oxidative damage through multi-pathway synergism, supporting its potential as a green and effective antioxidant feed additive in aquaculture.

The bisamide insecticides occupy a huge market share in the pesticide market and are commonly used in the integrated rice fish farming system. Most especially chlorantraniliprole (CAP) has been frequently used and detected in fish tissues. The 96-hr median lethal concentration (LC50) of seven bisamide insecticides, including tetrazoliumamide, fluorobenzamide, cyantraniliprole, tetrachloropamide, chlorantraniliprole, cyclobromide, and trifluorobenzine for fish, crab, and shrimp; closed shell organisms; zooplankton; and phytoplankton were determined. Results showed 96 hr-LC50 for fish, crab, and shrimp; closed shell organisms; zooplankton; and phytoplankton were 0.003∼5.263 mg·L-1, 0.0001∼1.562 mg·L-1, 0.010∼1.526 mg·L-1, 0.0004∼0.064 mg·L-1, respectively. The effects of 1.5 μg·L-1 CAP on enzymatic activities and gene expressions in juvenile American shad were simultaneously determined. Tumor necrosis factor-α, caspase-9 (except for 96 hr), interferon-γ and interleukin-10 significantly decreased, il1b significantly increased. The pathways of apoptosis, cytokine-cytokine receptor interaction, ferroptosis, mitogen-activated protein kinase signaling pathway, oxidative phosphorylation, p53 signaling pathway, and transforming growth factor-β signaling pathway, were significantly enriched in comparisons at 96 and 192 hr. Chlorantraniliprole induced changes in the enzymatic activities of inflammatory cytokines and gene expression profiles involving oxidative stress, apoptosis, and immune dysregulation in aquatic organisms.

To investigate the effects of natural salinity transition on megalopae of Eriocheir sinensis, this study systematically deciphered the response and adaptation mechanisms of megalopae to low-salinity stress. The results showed that the marine-to-freshwater habitat shift significantly reshaped the intestinal microbial community structure and increased the α-diversity index. The relative abundance of core bacterial taxa such as Amaricoccus was significantly elevated, while that of the conditional pathogen Flavobacterium was significantly reduced. At the host level, natural salinity transition stress triggered a series of profound cellular and molecular responses. To eliminate damaged cells, the Caspase-mediated apoptotic pathway and the LC3-mediated autophagic pathway were significantly activated. Meanwhile, signaling pathways controlling cell proliferation and growth, including Focal adhesion, Hippo, and PI3K-Akt, were significantly inhibited. Metabolically, stress response-related pathways such as Cortisol synthesis and secretion and AMP/Adenosine signaling were activated, driving an “energy-saving” strategy characterized by enhanced catabolism and reduced anabolism of proteins and lipids. Changes in the levels of key metabolites, such as 8-hydroxyguanosine and Ectoine, further confirmed the occurrence of oxidative stress and the shift in osmotic regulation strategies. Correlation analysis revealed that the Amaricoccus was significantly correlated with key genes involved in host amino acid metabolism, oxidative stress, and the PI3K-Akt pathway, indicating that microbe-host interactions play a central role in coordinating energy redistribution to cope with osmotic stress. This study reveals the multi-dimensional adaptation mechanisms through which megalopae achieve the transition from a hyperosmotic to a hypoosmotic environment by integrating microbial community reconstruction, precise cell clearance mechanisms, and systematic metabolic reprogramming.

PFOA and NPs are recognized as persistent organic pollutants with potential ecological risks in aquatic ecosystems, and they exhibit specific toxic effects on benthic invertebrates. As a vital respiratory organ of aquatic animals, the gill plays a key role in gas exchange and osmoregulation. However, studies on the potential adverse impacts of these two pollutants on the gill tissue remain scarce. In the present study, we conducted a 28-day stress experiment with the Eriocheir sinensis as a research model and systematically investigated the toxic effects of PFOA/NPs on gill organs by multi-omics sequencing. At the biochemical level, PFOA/NPs inhibited the activity and transcription of antioxidant enzymes (CAT, T-SOD, and GSH) or genes (gpx, gstd7), while triggering oxidative stress (MDA) and causing morphological damage. Moreover, PFOA/NPs induced inflammation (TNF-α, hil-6), apoptosis, autophagy (bnip3, stk17a, lc3a, epg5), suppression of immune responses (fcn, lyz), and disruption of glycolipid metabolism (fasn, acsl14, srebf1, acsly). In addition, the PFOA-NPs co-exposure disrupted the microbial flora structure in gill tissues, including reduced community evenness, increased dominance of specific species, and heightened abundances of both environmental organic pollutant-degrading microbes and opportunistic pathogens (Acidovorax, Sphaerotilus, Candidatus_Bacilloplasma). Furthermore, PFOA-NPs may disrupt microbial physiological homeostasis by suppressing the "LPS biosynthesis-antibiotic production-GAG degradation-lysosomal function" axis. These findings indicate that the gill organs of aquatic crustaceans are highly sensitive to organic pollutants such as PFOA and NPs, and long-term exposure disrupts their tissue physiology and microbial community homeostasis, thereby providing critical data to support the ecotoxicological assessment of PFOA/NPs in aquatic ecosystems.

The modern aquaculture is increasingly dependent on functional feeds, prophylactic formulations, and additives for water-quality regulation. However, the efficacy of many bioactive agents is constrained by multiple factors, including oxidative degradation with loss of activity, rapid dissolution and leaching in aquatic environments, and discrepancies between laboratory dosing protocols and on-farm feeding practices. Food-grade encapsulation technologies—such as micro-/nanoencapsulation, emulsions, liposomes, and hydrogel carriers—are now mature and can protect labile compounds while enabling controlled release. Their translation to aquaculture, nevertheless, requires targeted optimization that accounts for open-water exposure, mechanical stresses during feed processing, and pronounced interspecies differences in digestive physiology. This review synthesizes recent advances in food-grade carriers and fabrication processes relevant to aquaculture, emphasizing three priorities: (1) enhancing nutrient stability and controlled delivery; (2) improving mucosal targeting efficiency of oral vaccines and therapeutics; and (3) developing water-regulation functions using sustained-release nutrients and recyclable adsorbent materials. We further provide a critical assessment of key translational bottlenecks, including species-specific release kinetics, carrier aggregation and biofouling in complex aquatic matrices, life-cycle toxicological evaluation for non-target organisms, and constraints on cost and scalability for industrial deployment. Finally, we outline future priorities, including standardized in vitro digestion/leaching assays, cross-species benchmarking frameworks, and stimuli-responsive “smart” carriers to accelerate the transition from proof-of-concept to field-ready products.

All-trans retinoic acid (atRA) is known to regulate lipid metabolism, adipocyte differentiation, and the immune system in mammals and other aquatic species. However, studies on atRA in crustaceans, especially in Eriocheir sinensis, are still scarce. The present study aimed to investigate the regulatory effects of dietary or injected atRA on female crabs during the fattening period. In the dietary regulation experiment, 270 female crabs were fed diets containing different doses of atRA (0, 150, 300, 600, 1200, and 2400 mg/kg) for a total of 49 days. In the in vivo injection experiment, 90 females were divided into an experimental group (injected with a 0.3 μg/g dose of atRA) and a control group (injected with the same amount of DMSO solvent). Injections were given weekly throughout the 35-day experimental period. Results: Both dietary atRA and atRA injection promoted ovarian development, as evidenced by increased GSI, elevated serum Vg levels, decreased GIH, and upregulated expression of vg, vgr, and rxr genes. In terms of mechanism, dietary atRA promoted ovarian development via the upregulation of pyrimidine nucleotides and dehydroepiandrosterone, which supplied nucleic acid precursors and hormonal support. Furthermore, RXR was identified as a potential key target of atRA in inducing ovarian development, as molecular docking revealed that atRA could spontaneously bind to RXR. Moreover, following atRA injection, the expression of rxr, along with key genes involved in ovarian development, lipid synthesis, and lipid transport, was significantly upregulated. In addition, the atRA diet created a favorable microenvironment for ovarian development by reducing pro-inflammatory lipid levels in the ovary. Transcriptomic and metabolomic analyses revealed that atRA modulates energy and lipid metabolism by activating the AMPK pathway. In terms of the bacterial community structure, the atRA diet significantly decreased Fusobacterium abundance and enriched Parabacteroides as the signature beneficial bacterium. In terms of nutritional quality, the atRA diet markedly reduced saturated and trans-fatty acids while increasing monounsaturated fatty acids and various key essential amino acids. Conclusions: This study revealed that atRA plays a key role in promoting ovarian development, improving nutritional quality, and modulating the structure of the microbiota, thereby providing theoretical support for healthy aquaculture of female crabs during the fattening period.

The Chinese mitten crab, Eriocheir sinensis, is a water-dwelling crustacean that is widely distributed in northern hemisphere water systems. Body size is one of the crucial indicators determining the economic value of E. sinensis. However, research on the genetic basis and regulatory mechanisms of body size in this species is limited, with only a few relevant genes reported. Therefore, it is imperative to investigate the regulatory pathways associated with its growth. This study first utilized transcriptomic profiling and metabolomic sequencing to construct gene expression profiles and metabolite profiles of E. sinensis of different body sizes. Subsequently, through integrated omics analysis, the key genes and regulatory pathways involved in controlling the growth and size of crabs were preliminarily identified. This study found that larger female crabs exhibited significantly enhanced digestive functions, primarily reflected in the upregulation of trypsin-1 expression, suggesting its potentially pivotal role in regulating the growth and development of crabs. Interestingly, a variety of tissue-specific proteins such as APOLPP, RICK A, AGMO, and NEPHRIN, as well as REXO1L1P and ZCCHC24, indirectly influence the growth and development of crabs through their respective functional pathways. In addition, the key KEGG pathways, such as ECM-receptor interaction, cell adhesion, and the PI3K-Akt signaling pathway, were revealed to play central roles in the growth regulation of E. sinensis. These findings expand our understanding of the growth regulation mechanisms in crustaceans and offer potential molecular targets for body-size improvement in aquaculture.

Nanoplastics (NPs), the final form of degraded microplastics in the environment, can adsorb PFOA (an emerging organic pollutant in recent years) in several ways. Current research on these has focused on bony fishes and mollusks, however, the combined toxicity of PFOA and NPs remains unknown in Eriocheir sinensis. Therefore, the effects of single or combined exposure to PFOA and NPs were investigated. The results showed that NPs aggravated PFOA exposure-induced oxidative stress, serum lipid disorders, immune responses, and morphological damage. DEGs altered by NPs-PFOA exposure were predominantly enriched in GO terms for cell lumen, and organelle structure, and KEGG terms for spliceosome and endocrine disorders-related diseases. Notably, the apoptotic pathway plays a central role enriched under different exposure modes. PFOA or NPs-PFOA exposure disrupted the levels of lipids molecules-related metabolites by mediating the glycerophospholipid pathway, and the NPs mediated the ferroptosis pathway to exacerbate PFOA-induced metabolic toxicity. In addition, NPs exacerbated the inflammatory response and metabolic imbalance by mediating Fusobacterium ulcerans in the intestinal. In conclusion, this study provides a valuable reference for the characterization of NPs-PFOA combined pollution and a scientific basis for the development of environmental protection policies and pollution management strategies.

Silymarin has proven antioxidant activity and hepatoprotective effects, but no study to date has investigated the potential protective effect on deltamethrin-induced hepatopancreas injury in Chinese mitten crabs Eriocheir sinensis. This study investigated the protective effect of silymarin pretreatment on deltamethrin-induced hepatopancreas injury in E.sinensis. Healthy crabs (n = 150) were randomly divided into five experimental groups: the control, a deltamethrin exposure group (Basal feed without silymarin), and three silymarin groups (addition of 0.1, 0.5, or 1.0 g/kg diet to the basal feed). After 6 weeks of feeding (no deltamethrin exposure), the crabs were exposed to a deltamethrin concentration of 4.317 μg/L for 48 h. Histopathological results showed that the hepatopancreas remained relatively intact in the silymarin pretreatment groups. Furthermore, metabolites annotated by LC–MS were mainly enriched in signaling pathways related to cytochrome P450, terpenoid alkaloid biosynthesis and phospholipid metabolism. Silymarin at 0.1, 1.0 and/or 0.5 g/kg were significantly increased AKP, ACP, GSH activities and T-AOC levels, and significantly decreased AST, ALT, TNF-α, IL-6, NO, TC, MDA, CYP3A and CYP2E1 levels (P < 0.05). Silymarin at the concentation of 0.1, 0.5 and 1.0 g/kg could significantly up-regulated the expressions of immune-related genes (propo, alf3, crustin1, hsp70, hsp90, relish), anti-apoptotic gene (bcl-2), and significantly down-regulated the lipid metabolism-related genes (cpt1, srebp, acc) and apoptosis-related genes (caspase3, caspase8, p53, cyt-c) (P < 0.05). Silymarin at 0.5 and/or 1.0 g/kg significantly down-regulated the mRNA expression of inflammation-related genes (tnf-α, il-16) and drug metabolism-related genes (cyp2a, cyp2e1, cyp3a) (P < 0.05). The results demonstrate a good protective effect of 1.0 g/kg silymarin on deltamethrin-induced hepatopancreas injury induced by deltamethrin in a crustacean species.

This study employed multi-omics analysis to systematically evaluate the toxic effects of intraperitoneal injection of MC-LR on GIFT tilapia. The results showed that 96 h post injection, serum levels of aspartate GOT, GPT, LYZ, T-AOC, and SOD significantly decreased (p < 0.05). In contrast, hepatic levels of CAT and MDA significantly increased. The 16S rDNA sequencing method revealed a significant reduction in the α diversity of the intestinal microbiota. At the phylum level, the relative abundances of Firmicutes and Bacteroidota significantly decreased; at the genus level, several genera, including Bacteroides and Pseudomonas, also exhibited significant changes. Functional prediction indicated that the affected pathways were primarily related to metabolism and disease. Additionally, targeted metabolomics analysis showed a significant decrease in the levels of several SCFAs, such as butyric acid. Correlation analysis further elucidated the complex interactions between the intestinal microbiota, biochemical indicators, and SCFA metabolism. Overall, the study demonstrated that MC-LR induced oxidative stress and liver damage and led to intestinal microbiota imbalance and metabolic dysfunction in GIFT tilapia.

To investigate the potential toxic mechanism of Microcystin-LR (MC-LR) on juvenile Eriocheir sinensis (E. sinensis), a toxicity test was conducted by injecting MC-LR into the 3rd pereiopod. Following injection, we evaluated alterations in immune response biomarkers, antioxidant status, lipid metabolism-related genes expression, and intestinal microbiota composition in the hepatopancreas and intestinal tissues of E. sinensis. The results of immune response showed that after injection of MC-LR, the serum complement C3 level in E. sinensis significantly decreased at 48 hours (P < 0.05), whereas complement C4 level increased considerably from 12 to 96 hours (P < 0.01). The phenoloxidase system (PO) showed an increasing trend from 6 to 96 hours (P < 0.05 or P < 0.01). The levels of TNF-α, IL-6 significantly increased at 6 and 12 hours (P < 0.05 or P < 0.01). Gene expression analysis showed that FASN gene in the hepatopancreatic tissue displayed a higher expression at both 6 and 12 hours post-exposure (P < 0.01), while ALDH and ACAA2 gene exhibited a consistent downward trend from 6 to 48 hours (P < 0.05), Additionally, the mRNA levels of MECR and ACSL demonstrated a pattern of initial downregulation, followed by an upregulation, and subsequent downregulation. The antioxidant status results revealed that the levels GSH and CAT increased first and then decreased, while the activity of SOD decreased first and then increased. Meanwhile, the MDA content showed an increasing trend. 16 S rDNA analysis showed that the intestinal microbial diversity in MC-LR treatment group was significantly higher relative to the control group (P < 0.01). Compared with the control group, the MC-LR group had a significantly higher relative abundance of Proteobacteria, Fusobacteria, and Actinobacteria (P < 0.05) and a significantly lower relative abundance of Firmicutes (P < 0.01). At genus level, the relative abundance of Acinnetobacter, Flavobacterium, Acidovorax, Paracoccus, Cloacibacterium, Gemmobacter, Aeromonas, and Dechloromonas in the intestine of MC-LR-treated group was significantly increased relative to the control group (P < 0.05 or P < 0.01), but the relative abundance of Lachnospiraceae_NK4A136_group was significantly decreased (P < 0.01). The results of the study demonstrated that MC-LR could induced oxidative stress, hepatopancreas tissue damage, and intestinal microbial imbalance in E. sinensis.

There is limited knowledge about the toxicity of Microcystin-LR (MC-LR) in crustaceans, despite its high toxicity to aquatic organisms. This research aimed to explore the effects of MC-LR on cytotoxicity, oxidative stress, and apoptosis in the hepatopancreas of Eriocheir sinensis, as well as elucidate the involvement of reactive oxygen species (ROS) and potential mechanisms of toxicity. In vivo and in vitro exposures of crabs to MC-LR and N-acetylcysteine (NAC) were performed, followed by assessments of cell morphology, viability, tissue pathology, biochemical indicators, gene expression, and hepatopancreatic transcriptome. Results revealed that MC-LR facilitated the entry of the MC-LR transporter oatp3a into hepatopancreatic cells, leading to upregulated expression of phase I detoxification enzyme genes (cyp4c, cyp2e1, and cyp3) and downregulated the phase II enzyme genes (gst1, gpx, gsr2, gclc, and nqo1), resulting in increased ROS levels and cytotoxic effects. MC-LR exhibited cytotoxicity, reducing cell viability and inducing abnormal nuclear morphology with a 48 h-IC50 value of approximately 120 μm. MC-LR exposure caused biochemical changes indicative of oxidative stress damage and evident hepatopancreatic lesions. Additionally, MC-LR exposure regulated the levels of bax and bcl-2 expression, activating caspase 3 and 6 to induce cell apoptosis. Intervention with NAC attenuated MC-LR-induced ROS production and associated toxic effects. Transcriptome analysis revealed enrichment of differentially expressed genes in pathways related to cytochrome P450-mediated xenobiotic metabolism and the FoxO signaling pathway. These findings shed light on the potential mechanisms underlying MC-LR toxicity and provide valuable references for further research and conservation efforts regarding the health of aquatic animals.

The oxygen content in the fish ponds is facing greater challenges than before in the aquaculture of mandarin fish (Siniperca chuatsi) due to the change of climate and eutrophication. Until now, little is known about the molecular mechanisms underlying the harmful effects of hypoxia on this species. In this work, we built transcriptomes for the mandarin fish that were exposed to decreased oxygen concentration at two times points (24 h and 96 h). The respiratory metabolism activities of pyruvate kinase (PK), hexokinase (HK), lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) had different significantly changes during hypoxic treatment. Histological observation of the gill and brain also revealed some damages by hypoxia. A total of 196,355 transcripts were involved in the Gene Ontology analysis, and the numbers of differentially expressed genes (DEGs) in the brain and the gill between the control and experiment groups are 141 and 552 respectively involved in the different hypoxic stress time. The DEGs were then analyzed using KEGG enrichment analysis. The results showed significant differences in the expression of some genes involved in ribosome pathways,biosynthesis of amino acids, hippo signaling pathway, and pentose phosphate pathway,glycolysis/gluconeogenesis pathway and the TCA cycle. The huge number of transcriptome sequences collected in this study has enhanced the mandarin fish gene resources, and the identified DEGs and related pathway analysis give essential information for understanding biological responses to hypoxia.

This study investigated the toxicological mechanism of deltamethrin on Chinese mitten crab Eriocheir sinensis juveniles in fresh water. We first conducted an acute toxicity test, followed by laboratory methods to detect changes in immune-related indices in terms of antioxidant enzyme markers, lipid metabolism-related genes, and autophagy-related and apoptosis genes. The acute toxicity (96-h LC50) of deltamethrin to E. sinensis was 7.195 μg/L. After 48 h of exposure, serum showed elevated immune-related indices (P < 0.05) for alkaline phosphatase (AKP), acid phosphatase (ACP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), complement components C3 and C4, and the key pro-inflammatory cytokines interleukin-6, interleukin-1β, and tumor necrosis factor alpha (TNF-α). In hepatopancreas at 48 h, indicators related to the antioxidant system, namely superoxide dismutase (SOD) and glutathione (GSH), were significantly elevated, whereas nitric oxide and total antioxidant capacity (T-AOC) were decreased (P < 0.05). In contrast, lipid metabolism indices for triglyceride (TG), total cholesterol (TC), and malondialdehyde (MDA) were increased (P < 0.05). Transcriptomics and metabolomics revealed that exposure to deltamethrin disrupted the lipid metabolic process in the hepatopancreas mainly by altering fatty acid synthesis, amino acid metabolism, immune signaling, and autophagy activation, while the exposure increased the content of phospholipids and cholesterol but decreased the levels of amino acids and palmitoleic acid. Quantitative genetics revealed significantly aberrantly expressed (P < 0.05) lipid metabolism-related genes, including acc1, fasn, scd1, and pnpla2, all key genes involved in lipid accumulation. Deltamethrin exposure also significantly altered (P < 0.05) gene expression levels for Toll-like receptor (tlr), myeloid differentiation factor 88 (myd88), crustin1, anti-lipopolysaccharide factor isoform 3 (alf3), tumor necrosis factor alpha (tnf-α), and NF-κB transcription factor relish. Furthermore, deltamethrin activated the toll-like receptor/major myeloid differentiation response gene 88/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR/MyD88/NF-kB) signaling pathway, which activates a nonspecific immune response in E. sinensis. Additionally, carnitine palmitoyltransferase 1 A (cpt1a), cytochrome c (cyt-c), adenosine 5'-monophosphate (amp)-activated protein kinase (ampk), the autophagosomal protein microtubule-associated protein 1 light chain 3c (lc3c), and the autophagy-related proteins beclin1, atg5, atg12 were significantly induced (P < 0.05) in the adenosine monophosphate-activated protein kinase/rapamycin (AMPK/mTOR) signaling pathway. These changes resulted in excess free radicals, causing oxidative stress in the mitochondrial membrane, promoting mitochondrial autophagy. The results confirm that deltamethrin exposure can induce hepatopancreatic injury by promoting mitochondrial autophagy, activating an immune response, and inhibiting lipid metabolism. Overall, this study provides multi-level information to reveal the toxic effects of deltamethrin on E. sinensis.

The brain and liver of mandarin fish (Siniperca chuatsi) produce essential hormones for their growth and development. However, the mechanisms underlying the interplay of these hormones remain unclear. This study aimed to assess the slow - and fast-growing traits, including body weight and length of mandarin fish reared in a single pond. To compare the differentially expressed genes (DEGs) in slow - and fast-growing fishes, we performed RNA sequencing analysis. After assembling the clean reads, 192,280 transcripts and 100,416 unigenes were obtained. 344 and 845 DEGs in the brain and liver in the fast-and slow-growing group were annotated respectively. These DEGs were associated with signaling pathways involved in growth and development, such as AGE-RAGE, Transforming growth factor-beta/Smad, Mitogen-activated protein kinase, Wingless/Integrated, and Insulin-like growth factor (IGF) 1. Furthermore, our fasting experiment revealed a concurrent decrease in body weight and the expression levels of genes related to the growth hormone (GH)/IGF system, alongside an increase in the insulin-like growth factor binding protein gene IGFBP3 expression. These findings suggest the GH/IGF system regulates body weight during fasting periods. The vast amount of transcriptome data generated in this study substantially expands the existing gene and genome resources for the growth traits of mandarin fish.

Salvianolic acid B (Sal B), as one of the main water-soluble components of Salvia miltiorrhizae, has significant pharmacological activities, including antioxidant, free radical elimination and biofilm protection actions. However, the protective effect of Sal B on Nile tilapia and the underlying mechanism are rarely reported. Therefore, the aim of this study was to evaluate the effects of Sal B on antioxidant stress, apoptosis and autophagy in Nile tilapia liver. In this experiment, Nile tilapia were fed diets containing sal B (0.25, 0.50 and 0.75 g·kg−1) for 60 days, and then the oxidative hepatic injury of the tilapia was induced via intrapleural injection of 50 g·kg−1 cyclophosphamide (CTX) three times. After the final exposure to CTX, the Nile tilapia were weighed and blood and liver samples were collected for the detection of growth and biochemical indicators, pathological observations and TUNEL detection, as well as the determination of mRNA expression levels. The results showed that after the CTX treatment, the liver was severely damaged, the antioxidant capacity of the Nile tilapia was significantly decreased and the hepatocyte autophagy and apoptosis levels were significantly increased. Meanwhile, dietary Sal B can not only significantly improve the growth performance of tilapia and effectively reduce CTX-induced liver morphological lesions, but can also alleviate CTX-induced hepatocyte autophagy and apoptosis. In addition, Sal B also significantly regulated the expression of genes related to antioxidative stress, autophagy and apoptosis pathways. This suggested that the hepatoprotective effect of Sal B may be achieved through various pathways, including scavenging free radicals and inhibiting hepatocyte apoptosis and autophagy.

Environmental hypoxia is becoming more prevalent in aquatic environments of mandarin fish (Siniperca chuatsi) aquaculture because of eutrophication and climate change. Little information is available on the molecular mechanisms of the detrimental effects of hypoxia in this species. In this study, the authors assembled a transcriptome for mandarin fish exposed to lower oxygen conditions at different times (24 and 96 h). The antioxidant enzymatic activities of catalase, glutathione, superoxide dismutase, glutamic pyruvic transaminase and malondialdehyde significantly increased at 6 or 12 h but decreased after reaching a climax during 96 h hypoxia stress. The gene ontology study revealed 27,616 transcripts, whereas the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed 25 linked pathways. Significant changes in the expression of certain genes involved in protein processing in the endoplasmic reticulum, the calcium signalling system and inositol phosphate metabolism were discovered using the KEGG pathway analysis. In the liver, 97 genes were differentially expressed between the control and experimental groups. The expression level of 28 differentially expressed genes (DEGs) under different hypoxic stress conditions was detected using real-time PCR and compared to transcriptome sequencing results. The result showed that some genes in the experimental group associated with hypoxic stress, such as hif, ho-1a, ho-1b, igfbp1, hsp90 alpha and hsp90 beta, were significantly upregulated compared with those in the control group. The large amount of transcriptome data from this research has enlarged the mandarin fish gene and genome bioinformation. The identified DEGs and pathways are useful in further studies of biological responses to hypoxia.

Eriocheir sinensis is traditionally a native high-value crab that is widely distributed in eastern Asia, and the precocity is considered the bottleneck problem affecting the development of the industry. The precocious E. sinensis is defined as a crab that reaches complete sexual maturation during the first year of its lifespan rather than as normally in the second year. However, the exact regulatory mechanisms underlying the precocity are still unclear to date. This study is the first to explore the mechanism of precocity with transcriptome-metabolome association analysis between the precocious and normal sexually mature E. sinensis. Our results indicated that the phenylalanine metabolism (map00360) and neuroactive ligand-receptor interaction (map04080) pathways play an important role in the precocity in the ovary of E. sinensis. In map00360, the predicted aromatic-L-amino-acid decarboxylase and 4-hydroxyphenylpyruvate dioxygenase isoform X1 genes and the phenethylamine, phenylethyl alcohol, trans-2-hydroxycinnamate, and L-tyrosine metabolites were all down-regulated in the ovary of the precocious E. sinensis. The map04080 was the common KEGG pathway in the ovary and hepatopancreas between the precocious and normal crab. In the ovary, the predicted growth hormone secretagogue receptor type 1 gene was up-regulated, and the L-glutamate metabolite was down-regulated in the precocious E. sinensis. In the hepatopancreas, the predicted forkhead box protein I2 gene and taurine metabolite were up-regulated and the the L-glutamate metabolite was down-regulated in the precocious crab. There was no common pathway in the testis. Numerous common pathways in the hepatopancreas between male precocious and normal crab were identified. The specific amino acids, fatty acids and flavorful nucleotide (inosine monophosphate (MP), cytidine MP, adenosine MP, uridine MP, and guanosine MP) contents in the hepatopancreas and gonads further confirmed the above omics results. Our results suggest that the phenylalanine metabolism may affect the ovarian development by changing the contents of the neurotransmitter and tyrosine. The neuroactive ligand-receptor interaction pathway may affect the growth by changing the expressions of related genes and affect the umami taste of the gonads and hepatopancreas through the differences of L-glutamate metabolite in the precocious E. sinensis. The results provided valuable and novel insights on the precocious mechanism and may have a significant impact on the development of the E. sinensis aquaculture industry.