The experiment was aimed at examining the influence of adding emodin to feeds on the growth performance, liver immunity, and resistance against Aeromonas veronii infection among juvenile largemouth basses and other potential mechanisms. A total of 540 fish (45 ± 0.3 g) were randomly divided into 6 diets, including EM-0, EM-250, EM-500, EM-1000, EM-2000, and EM-4000 diets, in which 0, 250, 500, 1000, 2000, and 4000 mg kg⁻¹ emodin was added. Following a 60-day feeding test, it demonstrated that the feed conversion ratio (FCR) of juveniles within the EM-500 and EM-1000 groups remarkably exceeded that of the EM-0 group. Subsequently, unlike those in EM-0 group, the fish in the EM-1000 group showed heightened hepatocyte count, induced hepatic lipolysis-associated expression of peroxisome proliferators-activated receptor α (PPARα) and acyl-coenzyme an oxidase (ACO), and reduced the hepatic triglyceride (TG) levels. Additionally, EM-1000 could up-regulate the expressions of nuclear factor erythroid 2-associated factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in livers compared with controls and boost antioxidant enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), along with a lower content of reactive oxygen species (ROS) and malondialdehyde (MDA). Meanwhile, the EM-1000 group increased anti-inflammatory cytokines of interleukin-10 (IL-10) while suppressing the interleukin-8 (IL-8) expression of pro-inflammatory cytokines in livers by contrast to controls. In the end, juvenile largemouth bass in the EM-1000 group showed a comparatively highest survival rate, whereas fish in the EM-2000 and EM-4000 groups exhibited a little higher mortality than that of the EM-0 group. To sum up, our study exposed that supplementing emodin with 1000 mg kg⁻¹ in diet could enhance the hepatic antioxidant status and unspecific immunity to reinforce the protective effect on disease resistance, resulting in improving the growth performance in juvenile largemouth bass.

The effects of starvation and refeeding on the gut condition of juvenile largemouth bass (Micropterus salmoides) remain unclear. Therefore, our research aimed to explore these effects. Amylase and lipase activities were remarkably decreased in the starvation (ST) group, yet prominently increased in the refeeding (RE) group (p < 0.05). In addition to the malondialdehyde (MDA) level, catalase (CAT) and superoxide dismutase (SOD) activities were significantly upregulated in the ST group (p < 0.05) in marked contrast to those in the controls; however, the RE group showed no substantial variations in CAT and SOD activities or the MDA level (p > 0.05). During starvation, the expression of Nrf2-Keap1 pathway-associated genes was significantly upregulated (p < 0.05). The comparative levels of TNF-α, IL-1β, and IL-15 were highly increased, with the levels of TGF-β1 and IL-10 apparently downregulated in the ST group; in contrast, these levels were restored to their original values in the RE group (p < 0.05). In contrast to the controls, the ST group showed significantly lower height and width of the villi, muscle thickness, and crypt depth and a higher goblet cell number; however, these values were recovered to some extent in the RE group (p < 0.05). The dominant bacterial phyla in the intestines of both groups were Proteobacteria, Firmicutes, Bacteroidetes, Acidobacteria, and Actinobacteria, with marked inter-group differences in the genera Serratia and Lactobacillus. Metabolomics analysis showed that amino acid metabolism is disrupted during starvation and is restored after refeeding. In summary, this study expands our comprehension of the interaction between oxidative stress and antioxidant defenses among juvenile largemouth bass subjected to starvation and refeeding.

The microphthalmia-associated transcription factor (Mitf) family is central to melanocyte biology. Teleosts possess two mitf paralogs, mitfa and mitfb, yet their functional divergence remains incompletely understood. Here, we characterized the coding sequences, phylogeny, tissue distribution, developmental expression, cellular localization, and stress responsiveness of mitfa and mitfb in Congjiang natural mutant crucian carp (NMCC). Both genes encoded proteins containing the characteristic bHLH-ZIP domain. Phylogenetic analysis revealed that teleost mitfb clustered with the tetrapod mitf clade, indicating closer evolutionary affinity than mitfa. mitfa was predominantly expressed in skin and eyes, whereas mitfb showed broad tissue distribution. Both paralogs were constitutively expressed in skin across developmental stages; mitfa levels remained consistently lower than mitfb. Both transcripts were localized to melanocyte-containing regions of the skin. Transcriptomic analysis following high temperature (34 °C), UV radiation, and combined stress (48 h) revealed that mitfa was significantly upregulated by thermal stress, while mitfb showed no significant changes. Profiling of DNA damage response pathways uncovered extensive, stress-specific transcriptional remodeling. High temperature broadly suppressed apoptotic genes while upregulating tsc2, gadd45b, and cdip1; UV triggered widespread apoptotic gene activation. Combined stress elicited a hybrid signature. Notably, robust DNA Damage Response pathway remodeling contrasted with muted mitf responses, suggesting that DNA Damage Response-to-pigmentation signaling may operate predominantly at post-transcriptional levels. These findings reveal a substantial regulatory divergence between mitfa and mitfb, with mitfa maintaining a conserved melanogenic role while mitfb has been co-opted for broader functions in non-pigmentary tissues. The differential stress responses of the two paralogs further provide new insights into tissue-specific genotoxic stress signaling and melanogenic regulation in teleosts.

In order to investigate the molecular mechanisms of muscle fiber development underlying locomotion differences between two common carp (Cyprinus carpio) strains cultured in a rice-fish symbiosis system, we conducted comparative transcriptomic and proteomic analyses of muscle tissues collected from indolent Congjiang (CJ) and active FFRC No. 2 (FR) strains cultured under the identical paddy field conditions. RNA-seq revealed 3,708 differentially expressed genes (DEGs), while proteomic analysis identified 108 differentially expressed proteins (DEPs). Functional enrichment and protein-protein interaction (PPI) network analyses highlighted key genes (psma3, ppargc1a, ube3a) and proteins (Myh, Ckmt2b, Suclg2) involved in proteasome activity, adipocytokine signaling, and ubiquitin-mediated protein degradation. Quantitative real-time PCR (q-PCR) analysis of ubiquitin proteasome pathway related genes validated significantly elevated expression levels in the muscle tissue of CJ compared to FR. After a 21-day interference experiment, ube3a knockdown increased average muscle fiber area and diameter as well as reduced muscle fiber density in juvenile CJ, indicating that ube3a knockdown might promote muscle development in common carp. These results provided molecular insights into fish locomotion capacity related to behavioral adaptation in agroecological systems.

Nonylphenol (NP), a typical emerging pollutant, is widely detected in water bodies, yet its hepatotoxic mechanisms and mitigation strategies remain underexplored. This study evaluated the protective effects of a mixed probiotic (Lactobacillus acidophilus and Bacillus subtilis) against NP-induced hepatotoxicity in Silurus meridionalis by integrating transcriptomic and metabolomic analyses, with validation by RT-qPCR and ELISA. The results showed that NP exposure disrupted the arachidonic acid (AA) pathway (activating pro-inflammatory COX and LOX pathways while the suppressing anti-inflammatory CYP450 branch), promoted ferroptosis via iron dyshomeostasis and oxidative damage, and impaired triglyceride (TG) synthesis. Probiotic pretreatment reversed these toxic effects by modulating AA metabolism, suppressing COX (ptgs2a↓ → PGE₂↓) and LOX (alox12↓ → MDA↓) pathways, while upregulating the CYP450 pathway (cyp2j↑ → 11,12-EET↑). Probiotics also enhanced Fe³⁺ sequestration (steap4↑) and antioxidant defense (CAT↑, gpx4a↑), limiting Fenton reaction-mediated oxidative injury, and restored hepatic TG synthesis through upregulation of the DHAP-to-TG cascade (DHAP—(gpd1b↑) → G3P↑—(gpat3↑) → LPA—(agpat6↑) → PA—(plpp7↑) → DAG↑—(dgat2↑) → TG↑). These findings suggest that NP induces hepatotoxicity in S. meridionalis, involving ferroptosis, AA metabolism disruption and impaired TG synthesis as interconnected pathological events. Probiotics likely counteract this toxicity through systemic metabolic reprogramming. Collectively, these findings elucidate the hepatotoxic mechanisms of NP in S. meridionalis and offer toxicological data for its risk assessment, supporting the potential of probiotic-based strategies to mitigate emerging pollutant impacts in aquatic organisms.