Search

Ammonia toxicity in fish is closely related to ferroptosis, oxidative stress, and inflammatory responses. Iron is an essential trace element that plays a key role in many biological processes for cells and organisms, including ferroptosis, oxidative stress response, and inflammation. This study aimed to investigate the effect of iron on indicators of fish exposed to ammonia, specifically on the three aspects mentioned above. The head kidney macrophages of yellow catfish were randomly assigned to one of four groups: CON (normal control), AM (0.046 mg L -1 total ammonia nitrogen), Fe (20 μg mL -1 FeSO 4 ), and Fe + AM (20 μg mL -1 FeSO 4 , 0.046 mg L -1 total ammonia nitrogen). The cells were pretreated with FeSO 4 for 6 h followed by ammonia for 24 h. The study found that iron supplementation led to an excessive accumulation of iron and ROS in macrophages, but it did not strongly induce ferroptosis, oxidative stress, or inflammatory responses. This was supported by a decrease in T-AOC, and the downregulation of SOD, as well as an increase in GSH levels and the upregulation of TFR1, CAT and Nrf2. Furthermore, the mRNA expression of HIF-1, p53 and the anti-inflammatory M2 macrophage marker Arg-1 were upregulated. The results also showed that iron supplementation increased the progression of some macrophages from early apoptosis to late apoptotic cells. However, the combined treatment of iron and ammonia resulted in a stronger intracellular ferroptosis, oxidative stress, and inflammatory reaction compared to either treatment alone. Additionally, there was a noticeable increase in necrotic cells in the Fe + AM and AM groups. These findings indicate that the biological functions of iron in macrophages of fish may vary inconsistently in the presence or absence of ammonia stress., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Ammonia is one of the most serious environmental stressors which severely affect fishery production. Ammonia toxicity to fish has a tight relationship with oxidative stress, inflammation and ferroptosis (a type of programmed cell death characterized by iron-dependent lipid peroxidation), but the temporal response of the above three in brain remains unclear. In the present study, yellow catfish were exposed to three concentrations of ammonia: low concentration (TA-N ˂ 0.01 mg L -1 , LA), middle concentration (TA-N 5.70 mg L -1 , MA), high concentration (TA-N 28.50 mg L -1 , HA) for 96 h. Brain was selected as target tissues for analysis. Results showed that ammonia stress resulted in firstly increased contents of hydroxyl radical at 1 h, total iron at 12 h, malondialdehyde at 48 h, respectively, and decreased contents of GSH at 3 h. The initial high expression levels of ferroptosis (GPX4, system x c - , TFR1) and inflammatory-related factors (NF-ƙB p65, TNF, COX-2, and LOX-15B), antioxidant enzymes genes (SOD and CAT) were observed at first hour upon MA or HA stress. Combining all, it suggested that brain ferroptosis and inflammation were the first to be activated at the initial stage of ammonia stress, and then that provoked oxidative stress., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Ammonia is one of the most major pollutant and stress factors of aquaculture systems, and has seriously endangered fish health. However, few studies have been performed on mechanisms of the detrimental impact of ammonia stress and mitigation in fish. A study was carried out to investigate the response of genes involved in inflammation, antioxidation, polarization and apoptosis in head kidney macrophages to acute ammonia toxicity, and the alleviation effect of curcumin. The cells were divided into six groups, as follows: The control group composed of untreated macrophages (CON), the experimental groups, consisting of macrophages treated with 0.23 mg L -1 ammonia (AM), 45 μmol L -1 curcumin (CUR), 0.23 mg L -1 ammonia and 5 μmol L -1 curcumin (5A), 0.23 mg L -1 ammonia and 25 μmol L -1 curcumin (25A), 0.23 mg L -1 ammonia and 45 μmol L -1 curcumin (45A). The cells were pretreated with different concentrations of curcumin for 1 h and then incubated with ammonia for 24 h. The results showed that ammonia poisoning could increase ROS levels, up-regulate the expression of antioxidant enzymes (SOD and GPx), inflammatory cytokines (IL-1, IL-6 and TNF-α) and inflammatory mediators (NF-κB p65 and COX-2), decrease cell viability, down-regulate the expression of M2 marker (Arg-1) and anti-apoptosis (Bcl-2), but curcumin could alleviate the adverse effect of ammonia toxicity. Overall, these results have important implications for understanding of the mechanism of ammonia toxicity and the mitigating effect of curcumin in fish., (Copyright © 2021. Published by Elsevier Inc.)