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Hypoxia is a common phenomenon in aquaculture. With the dissolved oxygen (DO) 3.75 ± 0.25 mg O 2 /L for hypoxia group and 7.25 ± 0.25 mg O 2 /L for control group for 30, 60, and 90 days, long-term hypoxia stress was used to investigate the oxidative stress, apoptosis, and immunity in the intestine of Pelteobagrus vachelli. According to the results of measurement of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), and catalase (CAT) activities and malondialdehyde (MDA) content, the oxidative stress ability of the intestine was activated at 30 days and impaired at 60 and 90 days. The upregulation of Bcl-2-associated x (Bax); downregulation of B cell lymphoma-2 (Bcl-2); increased activities of caspase-3, caspase-9, and Na + -K + -ATPase; decreased activities of succinate dehydrogenase (SDH); and the release of cytochrome c (Cyt-c) in mitochondria revealed that hypoxia induced the apoptosis. Moreover, heat shock protein 70 (HSP 70), heat shock protein 90 (HSP 90), immunoglobulin M (IgM), and C-lysozyme (C-LZM) were activated to inhibit apoptosis, but the immunoregulatory function might be damaged at 60 and 90 days. This study provides a theoretical foundation for understanding the mechanisms of hypoxia stress and aquaculture management of P. vachelli., (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)

Water temperature is an important environmental factor in aquaculture farming that affects the survival and growth of organisms. The change in culture water temperature may not only modify various chemical and biological processes but also affect the status of fish populations. In previous studies, high temperature induced apoptosis and oxidative stress. However, the precise mechanism and the pathways that are activated in fish are still unclear. In the present study, we investigated the effects of high temperature (34°C) on the induction of apoptosis and oxidative stress in pufferfish (Takifugu obscurus) blood cells. The data showed that high temperature exposure increased oxygen species (ROS), cytoplasmic free-Ca(2+) concentration and cell apoptosis. To test the apoptotic pathway, the expression pattern of some key apoptotic related genes including P53, Bax, caspase 9 and caspase 3 were examined. The results showed that acute high temperature stress induced up-regulation of these genes, suggesting that the p53-Bax pathway and the caspase-dependent apoptotic pathway could be involved in apoptosis induced by high temperature stress. Furthermore, the gene expression of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT, GPx, and GR) and heat shock proteins (HSP90 and HSP70) in the blood cells were induced by high temperature stress. Taken together, our results showed that high temperature-induced oxidative stress may cause pufferfish blood cells apoptosis, and cooperatively activated p53-Bax and caspase-dependent apoptotic pathway., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Ammonia is one of major environmental pollutants in the freshwater aquatic system that affects the survival and growth of organisms. In the present study, we investigated the effects of ammonia exposure on apoptosis, oxidative stress and immune response in pufferfish (Takifugu obscurus). Fish were exposed to various concentrations of ammonia (0, 1.43, 3.57, 7.14mM) for 72h. The date showed that ammonia exposure could induce intracellular reactive oxygen species (ROS), interrupt intracellular Ca(2+) (cf-Ca(2+)) homeostasis, and subsequently lead to DNA damage and cell apoptosis. To test the apoptotic pathway, the expression patterns of some key apoptotic related genes including P53, Bax Bcl2, Caspase 9, Caspase 8 and Caspase 3 in the liver were examined. The results showed that ammonia stress could change these genes transcription, associated with increasing of cell apoptosis, suggesting that the P53-Bax-Bcl2 pathway and caspase-dependent apoptotic pathway could be involved in cell apoptosis induced by ammonia stress. In addition, ammonia stress could induced up-regulation of inflammatory cytokines (BAFF, TNF-α, IL-6 and IL-12) transcription, indicating that innate immune system play important roles in ammonia-induced toxicity in fish. Furthermore, the gene expressions of antioxidant enzymes (Mn-SOD, CAT, GPx, and GR) and heat shock proteins (HSP90 and HSP70) in the liver were induced by ammonia stress, suggesting that antioxidant system and heat shock proteins tried to protect cells from oxidative stress and apoptosis induced by ammonia stress. Our results will be helpful to understand the mechanism of aquatic toxicology induced by ammonia in fish., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Cadmium (Cd), a non-biodegradable contaminant in freshwater ecosystems, can pose a serious threat to aquatic animals at high levels. In this study, the Cd toxicokinetics and the immune and antioxidant defense were explored in Procambarus clarkii exposed to different levels of Cd (0, 0.1, 1.0 mg Cd/L) or treated with 1.0 mg Cd/L and dietary Bacillus subtilis supplementation (1 × 107 cfu/g). Results from the 21-day uptake and depuration experiment revealed that Cd exposure elicited a dose- and time-dependent uptake in all crayfish tissues, and the rank order of Cd concentration was gill > hepatopancreas > exoskeleton > muscle. The one-compartment model demonstrated that gills had the highest uptake rate (ku) value after Cd aqueous exposure and the ku and elimination rate (kd) values in gill, hepatopancreas, and exoskeleton of the group with 1.0 mg Cd/L were higher than those of the group at alow Cd concentration (0.1 mg Cd/L). However, B. subtilis could decrease Cd ku and increase Cd kd in hepatopancreas, resulting in the reduction of bioconcentration factors (BCF), steady-state concentrations (Css), and biological half-life (Tb1/2). A positive correlation was found between aqueous Cd concentration and the severity of hepatopancreas histopathological injury, while B. subtilis could ameliorate the pathological damage in the high Cd group. Similarly, aqueous exposure to Cd elevated malonaldehyde (MDA) content and suppressed the activities of lysozyme (LZM), acid phosphatase (ACP) in hepatopancreas and alkaline phosphatase (AKP) in hemolymph. The activities of superoxide dismutase (SOD) and catalase (CAT) in hepatopancreas were also inhibited. Nevertheless, they were all recovered with the dietary addition of B. subtilis. In conclusion, our results indicated that exposure to Cd significantly increased Cd accumulation and toxic damages in crayfish hepatopancreas, while dietary administration of B. subtilis to crayfish significantly decreased Cd accumulation and improved the immune and antioxidant defense, leading to the prevention in toxic effects of Cd. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) are ubiquitously present in the world's seas with unknown potential toxic effects on aquatic ecosystems. The aim of this study was to evaluate biochemical responses caused by 1–5 μm diameter plastic fluorescent red polymer microspheres (FRM), under short-term exposure of nauplii and juveniles of Artemia franciscana, using a set of biomarkers involved in important physiological processes such as biotransformation, neuronal transmission and oxidative stress. Two FRM concentrations (0.4 and 1.6 mg mL−1) present in the water at ecologically relevant concentrations were used to study their toxicity. No significant differences were found in growth, survival and feeding behaviour of nauplii, after 2 days of exposure to both FRM concentrations. However, in juveniles, survival decreased after 5 days of exposure to FRM1.6; but no significant differences were found in either growth or feeding behaviour. It was observed that nauplii and juveniles, under short-term exposure, had the ability to ingest and egest FRM particles, although their accumulation was higher in nauplii than in juveniles, maybe related with the capacity of the latter to empty their gut content faster, in the presence of food. Regarding biomarkers responses in nauplii, all enzymatic activities increased significantly, after short-term exposure to the higher FRM concentration tested (FRM1.6), which could be related with detoxifying MPs-triggered oxidative stress. In juveniles, the inhibition of ChE and the decrease in the activity of antioxidant enzymes, after 5 days of exposure to FRM1.6, might indicate a neurotoxic effect and oxidative damage induced by FRM. This study provides further evidences that accumulation of MPs in the gut by nauplii and juveniles of A. franciscana can induce negative effects on important physiological processes with influence on their health, highlighting the general concern about the negative effects of MPs pollution on aquatic species, as well as the need to understand the mechanism of MPs toxicity and its possible impacts on environmental safety. [ABSTRACT FROM AUTHOR]

An ammonia stress experiment was conducted by adjusting the concentration of total ammonia nitrogen (TAN) to 20 mg/L using ammonium chloride. The shrimp without ammonia stress was set as the control group. A total of 300 shrimp were randomly divided into six circular fiberglass tanks, each tank containing 50 shrimp. Antioxidant and immunological enzyme activities were investigated at five time points: 0 h, 12 h, 24 h, 48 h, and 96 h. The shrimp sampled at the initial time point were set as the control group. The samples used for intestinal microbiota determination were taken at two time points: 0 h and 96 h. All of the enzyme activities showed an initial increase followed by a decreasing trend. The enzyme activities (SOD, CAT, LZM, ACP, AKP) generally were higher at 12 h and 24 h compared to the control group, and then decreased some at 48 h and 96 h. The richness and diversity of intestinal microbiota decreased under ammonia stress. Proteobacteria, Firmicutes, and Bacteroidetes dominated in both the control and the 96-h group. Principal component analysis indicated a relatively small alteration of the microbiota by ammonia. Chitinophagaceae and Chloroflexi were the main species in the 96-h group, while Clostridium sensu stricto 1 and Paracoccus were the main species in the control group. Our findings suggest that ammonia exposure suppressed the antioxidant and immunological defenses of Litopenaeus vannamei. Ammonia exposure induced variation in the expression of intestinal microbiota abundance and composition, but the changes were unremarkable. [ABSTRACT FROM AUTHOR]

Recent studies on the effects of temperature on the antioxidant system of fish have been conducted mostly in vivo. In vivo experimental results are influenced by many factors, and can vary widely. Hence, experiments at the cellular level can provide a new direction for scientific research. The purpose of this study was to investigate the mechanism of the antioxidant system in response to temperature changes in grass carp Ctenopharyngodon idellus kidney (CIK) cells. CIK cells were exposed to culture temperatures of 20 °C, 24 °C, 28 °C, 32 °C, and 36 °C for 24 h, and the results showed that heat stress significantly increased the level of reactive oxygen species (ROS), which further led to increased content of malondialdehyde (MDA) and protein carbonyl. The increase of the ratio of Rh123 fluorescence indicated a decrease in mitochondrial membrane potential ( Δ Ψ m ), demonstrating that the changes in temperature destroyed the mitochondrial membrane of CIK cells. The acute temperature stress increased the activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and glutathione reductase (GR), and improved total antioxidant capacity (TAC) and glutathione (GSH). The relative mRNA expression levels of Cu–Zn sod, gpx, and cat were significantly increased with the variation in temperature. In conclusion, the changes in temperature disturbed the homeostasis of the CIK cells, destroyed the mitochondrial membrane, and enhanced the activity of major antioxidant enzymes to resist oxidative stress. [ABSTRACT FROM AUTHOR]

Ammonia is a pollutant frequently found in aquatic ecosystems. In fish, ammonia can cause physical damage, alter its behaviour, and even cause death. Exposure to ammonia also increases fish physiological stress, which can be measured through biomarkers. In this study, we analysed the effect of sublethal ammonia concentrations on the behaviour and the oxidative stress of Barbus meridionalis that had been pre-exposed to this compound in the wild. Wild-caught fish from a polluted site (pre-exposed fish) and from an unpolluted site (non-pre-exposed fish) were exposed, under experimental conditions, to total ammonia concentrations (TAN) of 0, 1, 5, and 8 mg/L. Swimming activity, feeding behaviour, and oxidative stress response based on biomarkers were analysed. Pre-exposed fish showed both an altered behaviour and an altered oxidative stress response in the control treatment (0 mg/L). Differences in swimming activity were also found as pre-exposed fish swam less. Lower feeding activity (voracity and satiety) and altered response to oxidative stress were also observed at ≥ 1 mg/L TAN. Biomarker results confirmed pre-exposed fish suffer from a reduction in their antioxidant defences and, hence, showed increased oxidative tissue damage. In summary, pre-exposed fish showed more sensitivity to ammonia exposure than fish from a pristine site. [ABSTRACT FROM AUTHOR]

Ammonia is the main environmental pollutant in aquaculture that has a negative impact on the healthy cultivation of common carp. The effects of antioxidant capacity, histopathology, and related gene expression of common carp (Cyprinus carpio) under ammonia stress (2.6 mM ammonia concentration, 168 h) were studied. In the study, ammonia stress can lead to oxidative stress in common carp, which is related to the regulation of SOD, GSH-PX, and CAT activities. Histopathology and TUNEL assays confirmed that apoptosis occurred in the hepatopancreas after ammonia stress, and the rate of apoptosis increased significantly with increasing exposure time (P < 0.05). We found the mRNA expression of p53, BAX, caspase-9, and caspase-3 were significantly enhanced (P < 0.05), and the transcriptional expression of BCL-2 was significantly inhibited (P < 0.05) in the late stage of ammonia exposure (96 h and 168 h). The results showed the apoptosis in the hepatopancreas of common carp under ammonia stress may be mediated by oxidative stress through the p53–BAX/BCL-2 apoptosis signal pathway. [ABSTRACT FROM AUTHOR]

Current study explored the acute toxicity and oxidative stress of ammonia-N on Macrobrachium rosenbergii. Prawns were exposed to ammonia-N at 3.01, 3.55, 4.18, 4.92, 5.80, 6.82, and 8.04 mg·L−1 for a 96 h acute toxicity test. In the subsequent sublethal toxicity text, they were exposed to ammonia-N at 0.5 or 1.88 mg·L−1 (1/2 96 h LC50) for 3, 8, 12, 24, 48, and 72 h. The total superoxide dismutase (T-SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) content were detected in the muscle, haemolymph, and gill. The gene expression of antioxidases (Cu/ZnSOD, CAT, GPX), heat shock proteins (HSP60, HSP70, HSP90), and apoptosis-related genes (Caspase 3, Bok) in the muscle and hepatopancreas also was evaluated. The LC50 values of non-ionic ammonia at 24, 48, 72, and 96 h were 7.72, 5.44, 4.28, and 3.78 mg·L−1, respectively. Ammonia-N significantly affected the T-SOD and CAT activities in the haemolymph and gill but not in the muscle. After 72 h of ammonia-N exposure, MDA content in the muscle, haemolymph, and gill in 1.88 mg·L−1 group significantly increased. The relative mRNA expression of antioxidant enzymes, heat shock proteins and Caspase 3 were upregulated in the hepatopancreas and muscle after ammonia exposure, especially in 1.88 mg·L−1. This result suggested that 1/2 96 h LC50 ammonia exposure induced severe oxidative stress, eventually even apoptosis of M. rosenbergii through the caspase pathway. Half of 96 h LC50 ammonia-N caused severe oxidative stress on M. rosenbergii. Ammonia-N induced the antioxidase and HSP to protect cells from oxidative stress. Ammonia-N induced mRNA expression level of Caspase 3 of M. rosenbergii. [ABSTRACT FROM AUTHOR]

Ammonia is one of the most common aquatic pollutants. To analyze the effect of ammonia exposure on the glutathione redox system, we investigated the levels of hydrogen peroxide (H2O2) and glutathione, and transcription and activities of glutathione-related enzymes in liver and gills of FFRC strain common carp (Cyprinus carpio L.) exposed to 0, 10, 20, and 30 mg/L of ammonia. The results showed that H2O2 content reached a maximum level at 48 h of exposure in the liver of fish. In gills, H2O2 increased rapidly at 6 h and reached to maximum levels at 24 h of exposure, indicating that gills experienced oxidative stress earlier than the liver of fish exposed to ammonia. Reduced glutathione (GSH) content and reduced glutathione/oxidized glutathione (GSH/GSSG) ratio increased significantly within 24 h of exposure. Meanwhile, the transcription and activities of glutathione S-transferase (GST) and glutathione reductase (GR) increased significantly in the liver, and glutathione peroxidase (GSH-Px) and GST increased in the gills of fish exposed to ammonia. Malondialdehyde (MDA) content kept at a low level after exposure to low concentration of ammonia, but increased significantly after exposure to 30 mg/L ammonia for 48 h along with a decrease in GSH content and GSH/GSSG ratio. These data showed that the glutathione redox system played an important role in protection against ammonia-induced oxidative stress in the liver and gills of FFRC strain common carp, though the defense capacity was not able to completely prevent oxidative damage occurring after exposure to higher concentration of ammonia. This research systematically studied the response of the glutathione redox system to ammonia stress and would provide novel information for a better understanding of the adaptive mechanisms of fish to environmental stress. [ABSTRACT FROM AUTHOR]

This study was conducted to determine the effects of vitamin E on growth performance, biochemical parameters, and antioxidant capacity of pufferfish (Takifugu obscurus) exposed to ammonia stress. The experimental basal diets supplemented with vitamin E at the rates of 2.31 (control), 21.84, 40.23, 83.64, 158.93, and 311.64 mg kg−1 dry weight were fed to fish for 60 days. After the feeding trial, the fish were exposed to 100 mg L−1 ammonia-nitrogen for 48 h. The results shown that the vitamin E group significantly improved weight gain, specific growth rate, and the expression levels of growth hormone receptors and insulin-like growth factor. Fish fed with the vitamin E-supplemented diets could increase plasma alkaline phosphatase activities and decrease plasma glutamicoxalacetic transaminase and glutamic-pyruvic transaminase activities. The relative expression levels of heat shock proteins (40.23-311.64 mg kg−1 vitamin E diet group), manganese superoxide dismutase (83.64-158.93 mg kg−1 vitamin E diet group), catalase (40.23-311.64 mg kg−1 vitamin E diet group), and glutathione reductase (40.23-311.64 mg kg−1 vitamin E diet group) were upregulated. On the other hand, the decreased level of reactive oxygen species (ROS) was observed in the 83.64-311.64 mg kg−1 vitamin E additive group. These results showed that vitamin E might have a potentially useful role as an effective antioxidant to improve resistance in pufferfish. [ABSTRACT FROM AUTHOR]

Ammonia is both a highly toxic environmental pollutant and the major nitrogenous waste produced by ammoniotelic teleosts. Although the acute toxic effects of ammonia have been widely studied in fish, the biochemical mechanisms of its toxicity have not been understood comprehensively. In this study, we performed comparative proteomic and metabolomic analysis between ammonia-challenged (1.2 and 2.6 mmol L−1 NH4Cl for 96 h) and control groups of marine medaka (Oryzias melastigma) to identify changes of the metabolite and protein profiles in response to ammonia stress. The metabolic responses included changes of multiple amino acids, carbohydrates (glucose and glycogen), energy metabolism products (ATP and creatinine), and other metabolites (choline and phosphocholine) after ammonia exposure, indicating that ammonia mainly caused disturbance in energy metabolism and amino acids metabolism. The two-dimensional electrophoresis-based proteomic study identified 23 altered proteins, which were involved in nervous system, locomotor system, cytoskeleton assembly, immune stress, oxidative stress, and signal transduction of apoptosis. These results suggested that ammonia not only induced oxidative stress, immune stress, cell injury and apoptosis but also affected the motor ability and central nervous system in marine medaka. It is the first time that metabolomic and proteomic approaches were integrated to elucidate ammonia toxicity in marine fishes. This study is of great value in better understanding the mechanisms of ammonia toxicity in marine fishes and in practical aspects of aquaculture. [ABSTRACT FROM AUTHOR]

The administration of bone mesenchymal stem cells (BMSCs) could reverse experimental colitis, and the predominant mechanism in tissue repair seems to be related to their paracrine activity. BMSCs derived extracellular vesicles (BMSC-EVs), including mcirovesicles and exosomes, containing diverse proteins, mRNAs and micro-RNAs, mediating various biological functions, might be a main paracrine mechanism for stem cell to injured cell communication. We aimed to investigate the potential alleviating effects of BMSC-EVs in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Intravenous injection of BMSC-EVs attenuated the severity of colitis as evidenced by decrease of disease activity index (DAI) and histological colonic damage. In inflammation response, the BMSC-EVs treatment significantly reduced both the mRNA and protein levels of nuclear factor kappaBp65 (NF-κBp65), tumor necrosis factor-alpha (TNF-α), induciblenitric oxidesynthase (iNOS) and cyclooxygenase-2 (COX-2) in injured colon. Additionally, the BMSC-EVs injection resulted in a markedly decrease in interleukin-1β (IL-1β) and an increase in interleukin-10 (IL-10) expression. Therapeutic effect of BMSC-EVs associated with suppression of oxidative perturbations was manifested by a decrease in the activity of myeloperoxidase (MPO) and Malondialdehyde (MDA), as well as an increase in superoxide dismutase (SOD) and glutathione (GSH). BMSC-EVs also suppressed the apoptosis via reducing the cleavage of caspase-3, caspase-8 and caspase-9 in colitis rats. Data obtained indicated that the beneficial effects of BMSC-EVs were due to the down regulation of pro-inflammatory cytokines levels, inhibition of NF-κBp65 signal transduction pathways, modulation of anti-oxidant/ oxidant balance, and moderation of the occurrence of apoptosis. [ABSTRACT FROM AUTHOR]

The residual contaminators such as ammonia and nitrite are widely considered as relevant sources of aquatic environmental pollutants, posing a great threat to shrimp survival. To study the toxicological effects of ammonia and nitrite exposure on the innate immune response in invertebrates, we investigated the oxidative stress and apoptosis in haemocytes of freshwater prawn ( Macrobrachium rosenbergii) under isolated and combined exposure to ammonia and nitrite in order to provide useful information about adult prawn immune responses. M. rosenbergii (13.44 ± 2.75 g) were exposed to 0, 5, and 25 mg/L total ammonia-N (TAN) and 0, 5, and 20 mg/L nitrite-N for 24 h. All ammonia concentrations were combined with all nitrite concentrations, making a total of nine treatments studied. Following the exposure treatment, antioxidant enzyme activity, reactive oxygen species (ROS) generation, nitric oxide (NO) generation, and apoptotic cell ratio of haemocytes were measured using flow cytometry. Results indicated that ROS generation was sensitive to the combined effect of ammonia and nitrite, which subsequently affected the Cu-Zn SOD activity. In addition, CAT showed the highest activity at 5 mg/L TAN while GPx decreased at 5 mg/L TAN and returned towards baseline at 25 mg/L. NO generation synchronized with the apoptotic cell ratio in haemocytes, indicating that NO production was closely associated with programmed cell death. Both NO production and apoptotic ratios significantly decreased following 25 mg/L TAN, which may be due to the antagonistic regulation of NO and GPx. We hypothesized that the toxicological effect of nitrite exhibited less change in physiological changes compared to that of ammonia, because of the high tolerance to nitrite exposure in mature M. rosenbergii and/or the competitive effects of chloride ions. Taken together, these results showed that ammonia and nitrite caused a series of combined oxidative stress and apoptosis in M. rosenbergi, but further studies are of great need to explain the mechanisms. [ABSTRACT FROM AUTHOR]

This study investigated the effect of continuous temperature decrease on hemocyte apoptosis of the white shrimp Litopenaeus vannamei. In the stress group, water temperature decreased from 26 to 17 °C at a rate of 1 °C/h. Shrimp kept at 26 ± 0.5 °C were used as control group. Total hemocyte count (THC), reactive oxygen species (ROS) production, cytoplasmic free-Ca (CF-Ca) concentration, mitochondrial membrane potential (MMP), apoptotic cell ratio, and caspase-3 activity of L. vannamei hemocytes were determined when water temperature decreased to 23, 20, and 17 °C, respectively. Increased ROS production in hemocytes was observed when water temperature decreased to 20 and 17 °C. Decreased THC and cellular MMP, increased CF-Ca concentration, apoptotic cell ratio, and caspase-3 activity were shown when water temperature decreased to 17 °C. These results indicate that water temperature decrease can induce oxidative stress on shrimp hemocytes and then cause mitochondria and caspase-3 mediated hemocyte apoptosis and THC reduction, when water temperature decreased to an unconformable level. [ABSTRACT FROM AUTHOR]