期刊
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
卷 243, 期 -, 页码 -出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpc.2021.108978
关键词
Ammonia stress; Hematological parameters; Oxidative stress; Inflammatory cytokines; Takifugu rubripes
资金
- National Key Research and Development Program of China [2017YFD0701701, 2019YFD0900503]
- Central Public-Interest Scientific Institution Basal Research Fund, YSFRI, CAFS [20603022018015]
- Key Laboratory of Mariculture & Stock Enhancement in North China's Sea, Ministry of Agriculture and Rural Affairs, Dalian Ocean University, P. R. China [2018-KF-02]
- Modern Agriculture Industry System Construction of Special Funds [CARS-47]
Ammonia exposure in Takifugu rubripes resulted in reduced hematological parameters, altered plasma components, increased antioxidant enzyme levels, and elevated heat shock protein expression, ultimately leading to an inflammatory response. This study sheds light on the mechanisms involved in ammonia-induced aquatic toxicology in marine fish, providing valuable insights for their captive management.
Ammonia is a major pollutant in aquatic environments and poses a considerable threat to the survival of fish. In this study, we investigated the toxic effects of ammonia on the hematological and biochemical parameters, oxidative stress, and immune responses in Takifugu rubripes. Juvenile T. rubripes (average weight 246.17 +/- 3.54 g) were exposed to different concentrations of ammonia (0, 5, 50, 100, and 150 mg/L) for 96 h. The results showed that the hematological parameters (hemoglobin, hematocrit, red blood cell, and white blood cell count) were significantly reduced in response to ammonia exposure. Of the plasma components, such as serum total protein, albumin, glucose, glutamic-oxalacetic transaminase, and glutamic-pyruvic transaminase, were significantly altered in response to ammonia exposure. Additionally, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx) were increased after exposure to low concentration ammonia exposure. However, when fish were exposed to a high concentration of ammonia, these parameters showed the opposite trend, suggesting that an increase in antioxidant enzymes during the early stages of ammonia exposure may contribute to the removal of the induced reactive oxygen species (ROS) and protect the cells from oxidative damage. However, as the ammonia concentration and exposure time increased, the overproduction of ROS accelerated the depletion of antioxidant enzymes. Ammonia exposure significantly increased the expression of heat shock proteins (HSP70 and HSP90). Ammonia poisoning elevated gene expressions of TLR-3, TNF-alpha, IL-6, IL-12, and IL-1 beta in the gills, causing an inflammatory response. Our findings provide new insights into the mechanisms involved in ammonia-induced aquatic toxicology in marine fish, which may aid in their captive management.
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