Crustaceans have a more persistent starvation tolerance than mammals, birds, reptiles, and even fish. This study is aimed at assessing the survival strategy and regulatory mechanism of crustaceans in response to starvation through an animal model using Eriocheir sinensis. In the 42-day starvation experiment, the hepatopancreas was found to become the target organ, which was characterized by atrophy of the thin wall in the hepatic tubules and expansion of the lumen. During short-term starvation, E. sinensis activates lipid and glycogen metabolism in the hepatopancreas with lipid metabolism dominating. In lipid metabolism, there was a significant decline in triglyceride, whereas cholesterol did not change significantly. Meanwhile, the fatty acid metabolism pathway was inhibited, but autophagy increased in the hepatopancreas, which may be the selective pathway for the decomposition of intracellular substances. However, under long-term starvation, the stored energy in the hepatopancreas was depleted, and E. sinensis selects to consume hepatopancreatic cells and maintain energy metabolism through apoptosis, which was triggered by both the death receptor pathway and the mitochondrial pathway. In addition, cell proliferation was blocked to reduce unnecessary energy consumption.

Cadmium (Cd) causes a broad spectrum of toxicological effects to animals. Aquatic animals were more likely to accumulate Cd than terrestrial animals because of the living environment. Clearance of Cd in aquatic animals has become an important part of aquatic food safety. The present study was focused on the oxidative damage induced by Cd in the liver of grass carp Ctenopharyngodon idellus and the protective effect of vitamin E (VE) and metallothionein (MT). Grass carp were divided into four groups: the control group, Cd+phosphate-buffered saline (PBS) group, Cd+VE group, and Cd+MT group. All fish were injected with CdCl₂ on the first day and then VE, MT, and PBS were given 4 days after injection, respectively. The liver function and antioxidant capacity of grass carp were evaluated. Cd administration resulted in damage of liver function and morphology in liver, which was expressed as the increased content of AST and ALT, rupture of organelles, and decrease of CAT, SOD, and GSH-Px activity. However, VE and MT treatments protected against Cd-induced damage of liver in grass carp by decreasing AST and ALT content, repairing organelles, and maintained the antioxidant system by elevating CAT, SOD, and GSH-Px activity and regulating related mRNA transcript expression. The results revealed that VE and MT might play an important role in the treatment of heavy metal poisoning through their antioxidative effects.

Interleukin-1β (IL-1β), interleukin-6 (IL-6), and serum amyloid A (SAA) are key pro-inflammatory mediators in the regulation of immune responses. The hypothesis posits that their expression varies with the progression of Ichthyophthirius multifiliis (Ich) infection and may serve as predictors of disease outcome. To elucidate their spatiotemporal dynamics, the full-length CDS of IL-1β, IL-6, and SAA in Pelteobagrus vachelli were cloned, and then their mRNA levels were tracked from infection onset (day 0) to resolution (day 40) or mortality in seven tissues. Key findings revealed a surge in IL-1β expression in the kidney and SAA expression in the spleen at 5 days post-infection (dpi), coinciding with no visible symptoms. Significant SAA elevation in the head kidney was observed at 10 dpi, preceding the emergence of white spots on the skin. This was followed by gill-specific SAA downregulation at 20 dpi, when 40% of fish presented with white spots. Complete clinical resolution by 40 dpi correlated with reduced hepatic SAA and branchial IL-1β levels. Notably, the concurrent upregulation of all three mediators occurred exclusively in the skin of moribund individuals. These findings identify potential biomarkers for tracking host inflammatory responses in ichthyophthiriasis.

In the context of host-microbe interactions, the microenvironment plays a critical role in facilitating microbial survival, and variations in these microenvironments may influence the pathogenicity of microorganisms. Vibrio mimicus , a major pathogen responsible for infections in aquatic animals, poses a substantial threat to yellow catfish ( Pelteobagrus fulvidraco ) and grass carp ( Ctenopharyngodon idella ), two naturally occurring hosts displaying markedly different susceptibility levels. This study aims to unravel the underlying mechanisms behind this susceptibility discrepancy in the two teleost species. Employing metabolomic analysis, we identified a distinctive microenvironment in yellow catfish, characterized by abundant purine nucleotides and oligopeptides. Furthermore, a total of 67 specific metabolites were identified from both yellow catfish and grass carp, with 33 displaying heightened expression on the body surface of yellow catfish, including nucleotides, amino acids, and gangliosides, while 34 were predominantly expressed on the body surface of grass carp, primarily comprising lipids. Subsequent investigations revealed that certain compounds related to nucleotides and oligopeptides exhibited significant growth-promoting effects and were utilized by V. mimicus as nutrients, with deoxyguanosine proving to be notably more than twice as effective as glucose. Moreover, during V. mimicus infection, numerous metabolites such as oligopeptides, purine nucleotides, and specific metabolites experienced considerable depletion in the skin of yellow catfish. Concurrently, several genes associated with nucleosidase and peptidase were upregulated in the skin and muscles of infected fish. These findings suggest that the microenvironment provided by different hosts plays a pivotal role in determining the infectivity of the pathogen. Additionally, our results indicate that the microenvironment on the surface of yellow catfish, characterized by an abundance of purine nucleotides and oligopeptides, indirectly enhances V. mimicus growth, ultimately augmenting its infectivity.