High-temperature stress response in the liver of Trachinotus ovatus: a cascade of oxidative stress, immunity, and bile acid metabolic reprogramming.
- 1State Key Laboratory of Mariculture Biobreeding and Sustainable Goods, Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, 510300, PR China.
- 2College of Fisheries and Life Science, Shanghai Ocean University, Shanghai, 201306, China.
- 3State Key Laboratory of Mariculture Biobreeding and Sustainable Goods, Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, 510300, PR China. [email protected].
Abstract
Fish exhibit a high degree of susceptibility to shifts in thermal conditions within the water. The liver is central to metabolic homeostasis and immune defense, and its physiological stability is critical for fish health. The present study evaluated the hepatic physiological responses of Trachinotus ovatus following a 7-day exposure to high-temperature (HT) stress, including alterations in histology, oxidative stress, iron homeostasis, inflammation, immunity, apoptosis, and bile acid (BA) metabolism. HT stress induced alterations in liver histology and disrupted redox homeostasis, accompanied by enhanced Nrf2-mediated antioxidant signaling and changes in antioxidant defense enzyme activities and peroxide levels. Iron homeostasis and lipid peroxide defense exhibited complex alterations, including Fe levels and NCOA4 expression were increased, accompanied by compensatory upregulation of iron-homeostasis genes (FTH1, FPN1, and NFS1) and antioxidant defense genes (GPx4, SLC7A11, and p53). However, reduced lipid peroxidation products (LPO and MDA) suggested that these changes reflected regulatory adaptation rather than the execution of ferroptosis. HT stress induced hepatic inflammatory and immune responses, characterized by activation of pro-inflammatory signaling, dysregulated anti-inflammatory regulation, downregulation of IL-8 expression, and downregulation of the immunoglobulin genes IgM and IgT. Apoptosis-related genes showed divergent expression patterns, with CHOP, Casp-9, and Casp-3 being upregulated, whereas CytC was downregulated. Furthermore, BA metabolism was affected, as shown by reductions in total BA pool size and free BA levels, along with the upregulated expression of BA metabolism-related genes (FXR, SULT1, and UGT8). Three metabolites, cholic acid, chenodeoxycholic acid, and 7-ketolithocholic acid were identified as potential biomarkers. Collectively, these findings suggest that HT stress impaired hepatic physiological homeostasis in T. ovatus, accompanied by tissue architecture disruption, redox imbalance, inflammatory responses, immune suppression, BA metabolic remodeling, and coordinated changes in iron homeostasis and apoptosis-related regulatory pathways.
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BibTeX
@article{zhu2026hightemperature,
title = {{High-temperature stress response in the liver of Trachinotus ovatus: a cascade of oxidative stress, immunity, and bile acid metabolic reprogramming.}},
author = {Ruijie Zhu and Meng Xiao and Xiaohua Huang and Dianchang Zhang and Falin Zhou and Yukai Yang and Huayang Guo and Yafei Duan},
journal = {Stress biology},
year = {2026},
month = oct,
doi = {10.1007/s44154-026-00344-y},
url = {https://europepmc.org/article/MED/42895594},
note = {CC BY},
}
RIS
TY - JOUR
TI - High-temperature stress response in the liver of Trachinotus ovatus: a cascade of oxidative stress, immunity, and bile acid metabolic reprogramming.
AU - Ruijie Zhu
AU - Meng Xiao
AU - Xiaohua Huang
AU - Dianchang Zhang
AU - Falin Zhou
AU - Yukai Yang
AU - Huayang Guo
AU - Yafei Duan
PY - 2026
DA - 2026/10/19
JO - Stress biology
DO - 10.1007/s44154-026-00344-y
UR - https://europepmc.org/article/MED/42895594
AB - Fish exhibit a high degree of susceptibility to shifts in thermal conditions within the water. The liver is central to metabolic homeostasis and immune defense, and its physiological stability is critical for fish health. The present study evaluated the hepatic physiological responses of Trachinotus ovatus following a 7-day exposure to high-temperature (HT) stress, including alterations in histology, oxidative stress, iron homeostasis, inflammation, immunity, apoptosis, and bile acid (BA) metabolism. HT stress induced alterations in liver histology and disrupted redox homeostasis, accompanied by enhanced Nrf2-mediated antioxidant signaling and changes in antioxidant defense enzyme activities and peroxide levels. Iron homeostasis and lipid peroxide defense exhibited complex alterations, including Fe levels and NCOA4 expression were increased, accompanied by compensatory upregulation of iron-homeostasis genes (FTH1, FPN1, and NFS1) and antioxidant defense genes (GPx4, SLC7A11, and p53). However, reduced lipid peroxidation products (LPO and MDA) suggested that these changes reflected regulatory adaptation rather than the execution of ferroptosis. HT stress induced hepatic inflammatory and immune responses, characterized by activation of pro-inflammatory signaling, dysregulated anti-inflammatory regulation, downregulation of IL-8 expression, and downregulation of the immunoglobulin genes IgM and IgT. Apoptosis-related genes showed divergent expression patterns, with CHOP, Casp-9, and Casp-3 being upregulated, whereas CytC was downregulated. Furthermore, BA metabolism was affected, as shown by reductions in total BA pool size and free BA levels, along with the upregulated expression of BA metabolism-related genes (FXR, SULT1, and UGT8). Three metabolites, cholic acid, chenodeoxycholic acid, and 7-ketolithocholic acid were identified as potential biomarkers. Collectively, these findings suggest that HT stress impaired hepatic physiological homeostasis in T. ovatus, accompanied by tissue architecture disruption, redox imbalance, inflammatory responses, immune suppression, BA metabolic remodeling, and coordinated changes in iron homeostasis and apoptosis-related regulatory pathways.
SN - 2731-0450
ER -