Kai Zhang

Hypoxia is a common stressor in aquaculture and severely compromises the physiological health of fish. The present study investigated the expression pattern and transcriptional response of the sirt1 gene (sirtuin1) in yellow catfish (Pelteobagrus fulvidraco) under acute hypoxia stress. Sequence analysis of the yellow catfish sirt1 gene indicated that the Sirt1 protein exhibits a high degree of sequence conservation among vertebrates. Tissue distribution analysis under normoxic conditions revealed that sirt1 mRNA was most abundantly expressed in the brain and intestine of yellow catfish. Results from the hypoxia stress trial (dissolved oxygen 1.1 ± 0.2 mg/L) demonstrated that sirt1 was the most hypoxia-responsive member of the sirt family, being significantly upregulated approximately 4.5-fold at 12 h. Subsequent functional validation experiments showed that sirt1 expression was significantly decreased at 6 h of acute hypoxia; together with the marked upregulation at 12 h observed in the time-course experiment, this suggests that the response of sirt1 to acute hypoxia is time-dependent. On this basis, a bidirectional intervention was performed using small interfering RNA (siRNA)-mediated knockdown of sirt1 and resveratrol-mediated activation to analyze the effects of sirt1 on downstream gene expression and intestinal histopathology. The results showed that inhibition of sirt1 led to compensatory upregulation of pdk1, impairment of ampkα signaling and a further decrease in stat3 expression, and aggravated hypoxia-induced intestinal histological damage, whereas resveratrol pretreatment partially restored the expression of the related genes and alleviated tissue injury. These findings indicate that sirt1 is a transcriptionally responsive gene involved in the response of yellow catfish to hypoxia stress, and provide a reference for further investigation into hypoxia adaptation in yellow catfish.

Acute hypoxia stress poses a significant challenge in aquaculture, not only compromising gut health but also resulting in substantial economic losses. Using an integrated multi-omics approach, this study demonstrates that hypoxia severely disrupts the intestinal function of yellow catfish (Pelteobagrus fulvidraco), specifically manifesting as phospholipid metabolism disorders, inhibited fatty acid β-oxidation, reduced short-chain fatty acid (SCFA) synthesis, imbalanced gut microbiota (e.g., decreased levels of beneficial lactic acid bacteria Lactococcus and Clostridium sensu stricto 1), and downregulation of detoxification pathways mediated by cytochrome P450. Building upon the previously isolated and identified high-yield SCFA-producing probiotic Clostridium butyricum B3 from yellow catfish in early work, this research further investigated the efficacy and mechanisms of B3 supplementation in mitigating hypoxia-induced intestinal barrier damage in yellow catfish. The results indicated that the supplementation of C. butyricum B3, particularly at a dose of 3.0 × 10⁷ CFU/g, significantly reduced histological damage, enhanced the expression of key tight junction proteins (such as ZO-1 and Claudin), and modulated hypoxia-inducible factor signaling pathways (including HIF-1α, FIH, and PHD). Furthermore, the application of C. butyricum B3 restored microbial ecological balance by promoting the growth of beneficial bacteria like Cetobacterium and inhibiting potential pathogens such as Acinetobacter. In conclusion, these findings underscore the potential of C. butyricum B3 as a novel probiotic strategy for enhancing fish hypoxia tolerance and maintaining intestinal integrity, offering valuable insights for sustainable aquaculture practices.

The burgeoning global population and the increasing recognition of seafood’s nutritional value place unprecedented pressure on aquatic food systems

Anatoxin-a (ANTX-a), a potent neurotoxin produced by various cyanobacterial species, poses a serious threat to aquatic organisms. This study investigated the neurotoxicity of ANTX-a on juvenile Chinese mitten crab (Eriocheir sinensis). Different from previous studies on vertebrate models or fish liver toxicity, we focused on the microbiota–intestine–brain axis. Results demonstrated that ANTX-a exposure induced significant neurotoxicity, marked by the upregulation of apoptosis-related genes and disruption of neurotransmitter homeostasis. Transcriptomic analysis of thoracic ganglia revealed significant dysregulation of metabolic pathways, characterized by upregulated histidine metabolism (elevated histidine decarboxylase-like) and downregulated lipid metabolism (suppressed sphingomyelin phosphodiesterase-like). Additionally, increased intestinal histamine levels and elevated serum diamine oxidase activity indicated intestinal barrier damage. Intestinal microbiota analysis revealed that the abundance of nerve-related bacteria Tyzzerella and Clostridium sensu stricto 1 changed significantly. In summary, these findings indicate that ANTX-a induced neurotoxicity by affecting neurotransmitter systems and gut health, implicating the microbiota–intestine–brain axis. The results underscore the role of microbiota–intestine–brain communication in cyanotoxin toxicity within aquatic invertebrates and provide new insights into the ecotoxicological risks of cyanobacterial blooms in aquatic invertebrates.

Intestinal inflammation is a common challenge in intensive aquaculture, yet its pathogenesis remains unclear. While interleukin 22 (IL-22) is recognized as a critical regulator of cellular homeostasis during inflammation in higher vertebrates, its roles in fish are not well understood. This study established hypoxia-induced models in intestinal tissues and primary intestinal epithelial cells of yellow catfish to investigate the involvement of IL-22 in maintaining intestinal homeostasis. Results revealed that Pelteobagrus fulvidraco IL-22 ( Pf_ IL-22) was abundantly expressed in mucosal tissues, with the highest levels in the gill and intestine. Hypoxia induced pronounced intestinal injury, characterized by loosening of the lamina propria and extensive vacuolization, while activating hypoxia-inducible factor (HIF) signaling and markedly up-regulating IL-22 expression. IL-22 levels peaked at 24 h post-hypoxia, suggesting a role in early immune responses. Recombinant Pf_IL-22 also induced transcription of pro-inflammatory mediators, including IL-1β and tumor necrosis factor α (TNF-α), in primary intestinal epithelial cells, indicating a dual regulatory function in balancing protection and inflammation. Mechanistic analyses revealed that HIF-1α directly interacted with a hypoxia response element within the IL-22 promoter to drive transcription, as confirmed by dual-luciferase assays, electrophoretic mobility-shift assays, and HIF-1α knockdown. Silencing Pf_IL-22 significantly suppressed Th17 cell differentiation pathways, demonstrating its role in shaping downstream immune responses. These findings establish the HIF-1α/IL-22 axis as a key regulatory pathway modulating immune responses and alleviating intestinal inflammation, providing a basis for developing IL-22-targeted immunotherapies and selective breeding strategies in aquaculture.

Copper (Cu) is an important metal pollutant commonly found in aquatic environment owing to its inherent bioaccumulation and biomagnification potentials and long-term persistence in environmental compartments. The application of novel fabricated copper nanoparticles (Cu-NPs) has led to cytotoxicity in aquatic animals. However, the differences in underlying toxicity mechanisms between Cu-NPs and waterborne Cu (such as CuSO₄) remain unelucidated. Herein, the mechanisms underlying the CuSO₄/Cu-NPs-mediated perturbation of the hepatopancreatic mitochondrial function at different concentrations were investigated and compared. After exposing Eriocheir sinensis to 0 (control), 5, 50, and 500 μg/L CuSO₄ and 10 μg/L Cu-NPs for 21 days, hepatopancreases were retrieved. The results revealed that Cu-NPs or CuSO₄ (50 and 500 μg/L) induced ultrastructural damage following a time-dose effect, as indicated by swelling and degeneration of the lumen of hepatic tubules. Excess CuSO₄ or Cu-NPs exposure decreased the antioxidative capacity and led to the over-accumulation of mitochondrial ROS. Moreover, the mitochondrial membrane potential (ΔΨm) was reduced and apoptosis induced. Additionally, both CuSO₄ and Cu-NPs increased the numbers of mitophagosomes and the mRNA and protein levels of LC3B, and triggered mitophagy through PRKN-independent pathway; however, mostly the BNIP3L/Beclin1 pathway was involved in excess CuSO₄-induced mitophagy. Altogether, this study provides a basis for exploring Cu-mediated potential mitochondrial autophagy activation mechanisms and their effects on environmental toxicity.