Rainbow trout (Oncorhynchus mykiss) is one of the world's most widely farmed cold-water fish. However, the rise in water temperature caused by global warming has seriously restricted the development of rainbow trout aquaculture. In this study, we investigated the physiological responses in the liver of rainbow trout exposed to 20 ℃ and 24 ℃ and returning to the initial temperature (14 ℃) by combining biochemical analyses and UPLC-QTOF-MS metabolomics. The results of the biochemical analysis showed that serum aminotransferase, lysozyme, total bilirubin, alkaline phosphatase and liver superoxide dismutase, glutathione peroxidase, and malondialdehyde in rainbow trout under heat stress changed significantly. Even after the temperature recovery, some of the above indicators were still affected. Compared to the control group, 115, 130, and 121 differentially expressed metabolites were identified in the 20 ℃, 24 ℃, and recovery groups, respectively. Further pathway enrichment of these metabolites revealed that heat stress mainly affected the linoleic acid metabolism, α-linolenic acid metabolism, glycerophospholipid metabolism, and sphingolipid metabolism in the liver of rainbow trout, and continuously affected these metabolic pathways during the recovery period. Notably, the enrichment of glutathione metabolic pathways was consistent with the changes in glutathione peroxidase in the biochemical results. The results above suggest that heat stress can induce immune responses and oxidative stress inside the rainbow trout. After temperature recovery, some of the hepatic functions of fish return to normal gradually. The biochemical analysis and UPLC-QTOF-MS metabolomics tools provide insight into the physiological regulation of rainbow trout in response to heat stress.

The salinization of the water environment caused by human activities and global warming has increased which has brought great survival challenges to aquatic animals. Crucian carp (Carassius auratus) is an essential freshwater economic fish with superior adaptability to saline-alkali water. However, the physiological regulation mechanism of crucian carp adapting to saline-alkali stress remains still unclear. In this study, crucian carp were exposed to freshwater or 20, 40, and 60 mmol/L NaHCO₃ water environments for 30 days, the effects of saline-alkali stress on the kidney were evaluated by histopathology, biochemical assays and metabolomics analysis from renal function, antioxidant capacity and metabolites level. Our results showed different degrees of kidney damage at different exposure concentrations, which were characterized by glomerular atrophy and swelling, renal tubular degranulation, obstruction and degeneration, renal interstitial edema, renal cell proliferation and necrosis. Saline-alkali stress could change the levels of several physiological parameters with renal function and antioxidant capacity, including creatinine (CREA), urea nitrogen (BUN), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). In addition, metabolomics analysis showed that differential metabolites (DMs) were involved in various metabolic pathways, including phenylalanine, tyrosine, and tryptophan biosynthesis, aminoacyl-tRNA biosynthesis, purine metabolism, glycerophospholipid metabolism, sphingolipid metabolism, glycolysis/gluconeogenesis and the TCA cycle. In general, our study revealed that saline-alkaline stress could cause significant changes in renal function and metabolic profiles, and induce severe damage in the crucian carp kidney through destroying the anti-oxidant system and energy homeostasis, inhibiting protein and amino acid catabolism, as well as disordering purine metabolism and lipid metabolism. This study could contribute to a deeper understanding the adverse effects of saline-alkali stress on crucian carp kidney and the regulatory mechanism in the crucian carp of saline-alkali adaptation at the metabolic level.

Crystal symmetry matters: with the increase in the crystal symmetry from VO ₂ (B) to VO ₂ (M) and to VO ₂ (R), a dramatic decline in Raman enhancement on VO ₂ nanosheets is revealed through temperature-dependent Raman measurements.

The aims of this study is to explore the metabolomic biomarker and pathway changes in crucian under carbonate alkalinity exposures using high-throughput metabolomics analysis based on ultra-performance liquid chromatography-electrospray ionization-quadrupole time of flight-tandem mass spectrometry (UPLC-ESI-QTOF-MS) for carrying out adaptive evolution of fish in environmental exposures and understanding molecular physiological mechanisms of saline–alkali tolerance in fishes. Under 60 day exposure management, the UPLC-ESI-QTOF-MS technology, coupled with a pattern recognition approach and metabolic pathway analysis, was utilized to give insight into the metabolic biomarker and pathway changes. In addition, biochemical parameters in response to carbonate alkalinity in fish were detected for chronic impairment evaluation. A total of twenty-seven endogenous metabolites were identified to distinguish the biochemical changes in fish in clean water under exposure to different concentrations of carbonate alkalinity (CA); these mainly involved amino acid synthesis and metabolism, arachidonic acid metabolism, glyoxylate and dicarboxylate metabolism, pyruvate metabolism and the citrate cycle (TCA cycle). Compared with the control group, CA exposure increased the level of blood ammonia; TP; ALB; Gln in the liver and gills; GS; urea in blood, the liver and gills; CREA; CPS; Glu and LDH; and decreased the level of weight gain rate, oxygen consumption, discharge rate of ammonia, SOD, CAT, ALT, AST and Na⁺/K⁺-ATPase. At low concentrations, CA can change the normal metabolism of fish in terms of changing the osmotic pressure regulation capacity, antioxidant capacity, ammonia metabolism and liver and kidney function to adapt to the CA exposure environment. As the concentration of CA increases, various metabolic processes in crucian are inhibited, causing chronic damage to the body. The results show that the metabolomic strategy is a potentially powerful tool for identifying the mechanisms in response to different environmental exposomes and offers precious information about the chronic response of fish to CA.