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General view of the Cyprinus carpio secondary lamellae of the gill viewed by light microscopy: C. carpio exposed to normoxia (control; A), (B and C) hypoxic gill exposed to 1.8 mg O 2 /l for 21 days showing (EPL) epithelial lifting and (H) hyperplasia and (D) recovery gill for 7 days showing (N) necrosis. Haematoxylin and eosin stain; thickness 5-8 μm. Scale bars 50 μm.
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In fish, a complex set of mechanisms deal with environmental stresses including hypoxia. In order to probe the hypothesis that hypoxia-induced stress could be manifested in varieties of pathways, a model species, mirror carp (Cyprinus carpio), were chronically exposed to hypoxic condition (dissolved oxygen level: 1.80±0.6mg/l) for 21 days and subse...
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... gill morphology of the normoxic group exhibited the typical structure in which lamellae were lined by epithelial cells ( Figure 5A). After 21 days exposure to hypoxia, gills showed several notable histological alterations including lifting of lamellar epithelium, epi- thelial hyperplasia and necrosis in primary and secondary lamellae ( Figure 5B and C). ...
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... gill morphology of the normoxic group exhibited the typical structure in which lamellae were lined by epithelial cells ( Figure 5A). After 21 days exposure to hypoxia, gills showed several notable histological alterations including lifting of lamellar epithelium, epi- thelial hyperplasia and necrosis in primary and secondary lamellae ( Figure 5B and C). The magnitude of these changes decreased fol- lowing 7 days exposure to normoxia (recovery period). ...
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... magnitude of these changes decreased fol- lowing 7 days exposure to normoxia (recovery period). The recovery was, however, not complete within 7 days in normoxic condition and the histological alterations persisted in this group ( Figure 5D). Quantitative analysis for three main parameters (viz. ...
Citations
... Halting energyintensive genome duplication processes leverages time for macromolecular repair and allows for energy redirection [118]. Recovery from stressors on the other hand is accompanied by sustained repair processes [119], [120]. The ppp5c is a cross-tissue hub gene in our study involved in cell cycle arrest and DNA damage repair [121] shown dysregulated in sh under severe stress [122]. ...
... Halting energyintensive genome duplication processes leverages time for macromolecular repair and allows for energy redirection [118]. Recovery from stressors on the other hand is accompanied by sustained repair processes [119], [120]. The ppp5c is a cross-tissue hub gene in our study involved in cell cycle arrest and DNA damage repair [121] shown dysregulated in sh under severe stress [122]. ...
Coastal and estuarine environments are under endogenic and exogenic pressures jeopardizing survival and diversity of inhabiting biota. Information of possible synergistic effects of multiple (a)biotic stressors and holobiont interaction are largely missing in the Elbe estuary but are of importance to estimate unforeseen effects on animals’ physiology. Here, we seek to leverage host-transcriptional RNA-seq and gill mucus microbial 16S rRNA metabarcoding data coupled with physiological and abiotic measurements in a network analysis approach to deconvolute the impact of multiple stressors on the health of juvenile Sander lucioperca along one of the largest European estuaries. We find mesohaline areas characterized by gill tissue specific transcriptional responses matching osmosensing and tissue remodeling. Liver transcriptomes instead emphasized that zander from highly turbid areas were undergoing starvation which was supported by compromised body condition. Potential pathogenic bacteria, including Shewanella , Acinetobacter , Aeromonas and Chryseobacterium , dominated the gill microbiome along the freshwater transition and oxygen minimum zone. Their occurrence coincided with a strong adaptive and innate transcriptional immune response in host gill and enhanced energy demand in liver tissue supporting their potential pathogenicity. Overall, we demonstrate the information gain from integration of omics data into biomonitoring of fish and point out bacterial species with disease potential.
... Under hypoxia, HIF-1α can arrest the DNA replication process by interacting with the protein CDC6, which is essential for loading the MCM complex (which has DNA helicase activity) onto DNA (Huang, 2013;Hubbi et al., 2013). Additionally, HIF-1α could also mitigate oxidative DNA damage in carp by regulating the expression of its downstream target genes (OGG1 and XRCC1) (Mustafa et al., 2015). Given the common occurrence of DNA damage in rainbow trout and carps reared at hypoxic conditions described above, it is suggested that HIF-1α has a good potential for being an indicator or biomarker for monitoring heath status of aquatic species or developing molecular breeding strategies. ...
Hypoxia is a harmful result of anthropogenic climate change. With the expansion of global low-oxygen zones (LOZs), many organisms have faced unprecedented challenges affecting their survival and reproduction. Extensive research has indicated that oxygen limitation has drastic effects on aquatic animals, including on their development, morphology, behavior, reproduction, and physiological metabolism. In this review, the global distribution and formation of LOZs were analyzed, and the impacts of hypoxia on aquatic animals and the molecular responses of aquatic animals to hypoxia were then summarized. The commonalities and specificities of the response to hypoxia in aquatic animals in different LOZs were discussed lastly. In general, this review will deepen the knowledge of the impacts of hypoxia on aquaculture and provide more information and research directions for the development of fishery resource protection strategies.
... In the long evolutionary process, the tolerance of animals to environmental stress is compatible with the environment in which they live (Wu et al., 2014;Witt and Huerta-Sańchez, 2019). Qinghai-Tibet Plateau has extreme environmental conditions that are not available in low-altitude plain areas, plateau fish have acquired the ability to resist high-altitude environmental stress during long-term adaptive evolution (Zhuang et al., 2012;Little and Seebacher, 2013;Guan et al., 2014;Kültz, 2015;Mustafa et al., 2015;Sushchik et al., 2018;Nobrega et al., 2019;Evans and Kültz, 2020;Yuan et al., 2020). In this study, the stress experiments of low temperature, low oxygen, salinity and UVR were carried out. ...
The distribution pattern of species is determined by the environment and their adaptability to the environment. Qinghai-Tibet Plateau has become a natural laboratory for studying adaptive evolution due to its extreme environmental characteristics such as low temperature, low oxygen, high salinity and high ultraviolet radiation (UVR). Fish are sensitive to the environmental stress, so they are ideal materials for studying high-altitude adaptation of animals. Previous studies have mainly focused on the adaptability of plateau species, but the reasons why plain species cannot spread to the plateau have been ignored. In this study, stress experiments and histological experiments were used to compare the tolerance of six Barbini fishes (family: Cyprinidae) distributed at different altitudes and regions to low temperature, low oxygen, salinity and UVR. Results showed that the tolerance of fishes to high-altitude environmental stress factors was closely related to the environmental stress of their main habitats. The high-altitude fish Gymnocypris eckloni had strong tolerance to all stress factors, while the other five fishes from middle and low altitudes could not adapt to single or multiple stress factors, with significant interspecific differences. Among these factors, middle- and low-altitude fishes showed common low tolerance to UVR, suggesting that high UVR, the factor lacking at low altitude areas, plays an important role. Moreover, during the uplift of the Qinghai-Tibet Plateau, Schizothorax fish disappeared from the middle of the plateau. We speculate that this was caused by its intolerance to the increasingly extreme plateau environment, especially salinity.
... At the end of the experiment, three fish from each tank were selected randomly. Blood samples were collected from caudal vessel, blood parameters including red blood cells (RBC) and white blood cells (WBC) count were counted by Neubaur's upgraded haematocytometer (Marienfeld, Superior, Germany) using Deices as a diluting fluid (26,27). Hemoglobin content and hematocrit percentage were detected according to procedure of Al-Rudainy et al. (4). ...
In present study, we assessed the role of kaolin [(Al2Si2O5(OH)4), an inert clay], for treatment of common carp, Cyprinus carpio experimentally infected with Pesudomonas aeruginosa. Fish were experimentally challenged with P. aeruginosa (LD50= 2±0.2×109 CFU/ml), in untreated water or water treated with addition of kaolin at levels of 4, 6 and 8g/l (G1, G2 and G3 respectively). Over the 5‐day course of kaolin treatment led to significantly (P ≤ 0.05) improved of survival (100%) in treated groups (G2 and G3) as compared to untreated fish (infected group; 75% survival). Considerable changes were observed in blood parameters, leucocyte count recorded significant increase (P≤0.05) in G2 and G3 relative to C- and C+ groups. Erythrocyte count, Hb content and HT(%) reported significant decrease (P≤0.05) in all treated groups (G1, G2 and G3) related to C- group. Globulin level registered significantly increased (P≤0.05) in G2 and G3 than C+ group. The current study strongly recommends that treatment of common carp infected with kaolin at 6 and 8g/l improves survival, hematological and biochemical profile, against P. aeruginosa. Future complete molecular studies are required before application of kaolin as a treatment in aquaculture.
... These biological processes have been studied in hypoxia response in some other aquatic organisms, including Oryzias melastigma, 99 O. latipes, 100 Sillago sihama, 101 G. aculeatus, 102 Gillichthys mirabilis, 103 Fundulus grandis, 104 Micropogonias undulatus, 105 and Cyprinus carpio. 106,107 Pathways that are closely related to the glutamate− glutamine cycle, an important metabolic process in hypoxia responses of abalone mentioned in our previous study, 47 including nicotinate and nicotinamide metabolism; aminoacyl-tRNA biosynthesis; valine, leucine, and isoleucine degradation; ABC transporter; glutamatergic synapse; circadian entrainment; and long-term depression, are also enriched by upregulated and down-regulated SDEmRNAs in this study. ...
After being exposed to environmental stimuli during early developmental stages, some organisms may gain or weaken physiological regulating abilities, which would have long-lasting effects on their performance. Environmental hypoxia events can have significant effects on marine organisms, but for breeding programs and other practical applications, it is important to further explore the long-term physiological effects of early hypoxia exposure in economically significant species. In this study, the Pacific abalone Haliotis discus hannai was exposed to moderate hypoxia (∼4 mg/L) from zygote to trochophora, and the assessments of hypoxia tolerance were conducted on the grow-out stage. The results revealed that juvenile abalones exposed to hypoxia at the early development stages were more hypoxia-tolerant but with slower weight growth, a phenomenon called the trade-off between growth and survival. These phenotypic effects driven by the hypoxia exposure were explained by strong selection of genes involved in signal transduction, autophagy, apoptosis, and hormone regulation. Moreover, long non-coding RNA regulation plays an important role modulating carry-over effects by controlling DNA replication and repair, signal transduction, myocardial activity, and hormone regulation. This study revealed that the ability to create favorable phenotypic differentiation through genetic selection and/or epigenetic regulation is important for the survival and development of aquatic animals in the face of rapidly changing environmental conditions.
... Under chronic hypoxia, lipolysis replaces glycolysis, and lipids are the main energy source of fish (Li et al., 2018). Besides, both acute and chronic hypoxia stress promotes cell apoptosis and oxidative stress leading to DNA damage (Poon et al., 2007;Mahfouz et al., 2015;Mustafa et al., 2015;Birnie-Gauvin et al., 2017;Chowdhury and Saikia, 2020), weakens the innate immune system and makes fish more susceptible to pathogens (Giomi et al., 2016;Esteve et al., 2017;Sae-Lim et al., 2017;Abdel-Tawwab et al., 2019). Furthermore, fishes can show various behavioural responses such as rising to the surface to breathe the uppermost layer of water in contact with air, increasing activity to escape the hypoxic area or decreasing activity to reduce oxygen demand (Domenici et al., 2007;Domenici et al., 2013;Bowyer et al., 2014). ...
... Loss of smu1 function leads to multiple cellular defects, including chromosomal instability, aberrant DNA replication and alternative RNA splicing events. Accordingly, DNA damage is also closely linked to hypoxia, as was previously described in common carp and Nile tilapia (Poon et al., 2007;Mahfouz et al., 2015;Mustafa et al., 2015). Besides, the smu1 gene in zebrafish was upregulated under acute hypoxia (Ragsdale et al., 2020). ...
Hypoxia is one of the major threats to the aquaculture sector resulting in substantial economic losses to the fish farmers. Thus, tolerance to hypoxia is of high economic interest to be genetically improved by breeding programs. Rainbow trout (Oncorhynchus mykiss) is one of the most cultured salmonid species worldwide, with well-developed breeding programs. Still, studies of genetic potential to improve hypoxia tolerance in this species are rare. In the present study, 1320 individuals of rainbow trout were used for a genome-wide association study of acute hypoxia tolerance based on imputed high-density genotypes to explore the genetic architecture and related candidate genes affecting hypoxia response. Three significant (Omy31_1, Omy31_2, Omy20) and two putative (Omy15, Omy28) quantitative trait loci (QTLs) were detected, but each of them only explained between 0.2% and 0.8% of the genetic variance of acute hypoxia tolerance. However, heritability was estimated at a moderate value of 0.24–0.28, that suggests a solid potential to improve hypoxia tolerance in the studied rainbow trout population by genetic selection. Moreover, it was shown that genomic prediction for hypoxia tolerance would lead to a relative increase of ~11% for genomic selection (GS) accuracy compared to the pedigree-based selection, considering a reference population of 1000 individuals. Finally, fifteen genes (ids, fmr1, arx, lonrf3, commd5, map4k4, smu1, b4galt1, re1, abca1, noa1, igfbp7, noxo1, bcl2a, mylk3) were proposed as potential functional candidates involved in hypoxia tolerance. Taking all proposed candidate genes (6 out of 15 genes) and high linkage disequilibrium (r²) values within the main QTL (Omy31_1), we may hypothesize that the complex response to acute hypoxia in rainbow trout, i.e., the interplay between behavioural, morphological, and physiological responses, is primarily encoded by a supergene. However, further functional validation of their effects may help to specify the biological mechanisms triggering a response to acute hypoxia in rainbow trout.
... Uric acid was significantly more abundant under hypoxic conditions as compared to normoxia and reoxygenation, suggesting that hypoxia disrupted normal gill function, destabilized blood pressure, and increased oxidative stress. These results were consistent with a previous study of oxidative damage associated with hypoxia in carp [27]. In addition, it has been shown that, under hypoxic conditions, ATP in fish tissues is converted to adenosine and xanthine, depleting overall levels of ATP, which reduces the amount of energy available to the body. ...
Takifugu obscurus has relatively small gills and gill pores. Consequently, a relatively low respiratory capacity. This fish is thus easily negatively affected by the low levels of dissolved oxygen (DO) that are common in high-intensity aquaculture. In order to clarify the mechanisms underlying the hypoxia response of T. obscurus, we used liquid mass spectrometry (LC–MS) to identify and quantify the metabolites present in the T. obscurus gill under the following conditions: normoxia (DO, 7.0 ± 0.2 mg/L), hypoxia (DO, 0.9 ± 0.2 mg/L), and reoxygenation (4, 12, and 24 h after return to normoxia conditions). We identified a total of 821 and 383 metabolites in the gill in positive and negative ion modes, respectively. Of the metabolites identified in positive ion mode, 136 were differentially abundant between hypoxia and all other conditions; of the metabolites identified in negative ion mode, 34 were differentially abundant between hypoxia and all other conditions. The metabolites which were differentially abundant under hypoxia primarily included glycerol phospholipids, fatty acids, hormones, and amino acids as well as related compounds. The pathways which were significantly enriched in the differentially abundant metabolites included the lipid metabolism, amino acid metabolism, purine metabolism, FoxO signaling pathway, and mTOR signaling pathway. Our results help to clarify the mechanisms underlying hypoxia tolerance and to identify hypoxia-related metabolites, as well as to highlight potential research targets for the development of hypoxic-tolerant strains in the future.
... Hepatocytes can be a good indicator of oxidative stress in fish (Mustafa et al. 2015). We selected hepatocytes from P. lagowskii after 24-h hypoxia, 2 days of sustained hypoxia and diel-cycling hypoxia for the FISH analysis. ...
As an intermediate link between multiple cellular stresses and cellular responses, p53, together with its upstream and downstream regulators and related genes, constitutes a complex network that regulates cellular stresses and cellular responses. However, no studies have investigated p53 in Phoxinus lagowskii, particularly the expression of p53 under different hypoxic conditions. In the present study, the cDNA of p53 from the Phoxinus lagowskii was cloned by the combination of homology cloning and rapid amplification of cDNA ends (RACE) approaches. The full-length cDNA of Pl-p53 was 1878 bp, including an open reading frame (ORF) of 1116 bp encoding a polypeptide of 371 amino acids with a predicted molecular weight of 41.22 kDa and a theoretical isoelectric point of 7.38. Quantitative real-time (qRT) PCR assays revealed that Pl-p53 was commonly expressed in all tissues examined, with highest expression in the heart. In addition, we investigated the expression of Pl-p53 in different tissues under different hypoxic conditions. In the short-term hypoxia group, Pl-p53 expression was down-regulated in both the brain and heart. The Pl-p53 expression was significantly elevated at 6 h in the muscle and liver, and was significantly up-regulated at 24 h in spleen. These results suggest that Pl-p53 plays different regulatory roles and provide a theoretical basis for the changes of p53 in fish facing hypoxic environments.
... A disruption of the balance between the production of oxygen FRs because of an increased biosynthesis, intake of toxins that generate FRs, and the mechanisms that protect from oxidative damage has been suggested as a critical factor not just for normal aging but also for pathological processes of NDDs, especially for AD (Götz et al. 1994). If a small fluctuation in the steady-state concentration becomes uncontrollable, it may result in elevation of the steady-state concentration, initiating FR-mediated chain reactions which randomly target lipids (Rubbo et al. 1995), proteins (Stadtman and Levine 2000), polysaccharides (Kaur and Halliwell 1994), and even DNA (Mustafa et al. 2015). Thus, since the brain membrane phospholipids consist of polyunsaturated fatty acids, the brain becomes particularly vulnerable to FR damage. ...
Recent advancements and growing attention about free radicals (ROS) and redox signaling enable the scientific fraternity to consider their involvement in the pathophysiology of inflammatory diseases, metabolic disorders, and neurological defects. Free radicals increase the concentration of reactive oxygen and nitrogen species in the biological system through different endogenous sources and thus increased the overall oxidative stress. An increase in oxidative stress causes cell death through different signaling mechanisms such as mitochondrial impairment, cell-cycle arrest, DNA damage response, inflammation, negative regulation of protein, and lipid peroxidation. Thus, an appropriate balance between free radicals and antioxidants becomes crucial to maintain physiological function. Since the 1brain requires high oxygen for its functioning, it is highly vulnerable to free radical generation and enhanced ROS in the brain adversely affects axonal regeneration and synaptic plasticity, which results in neuronal cell death. In addition, increased ROS in the brain alters various signaling pathways such as apoptosis, autophagy, inflammation and microglial activation, DNA damage response, and cell-cycle arrest, leading to memory and learning defects. Mounting evidence suggests the potential involvement of micro-RNAs, circular-RNAs, natural and dietary compounds, synthetic inhibitors, and heat-shock proteins as therapeutic agents to combat neurological diseases. Herein, we explain the mechanism of free radical generation and its role in mitochondrial, protein, and lipid peroxidation biology. Further, we discuss the negative role of free radicals in synaptic plasticity and axonal regeneration through the modulation of various signaling molecules and also in the involvement of free radicals in various neurological diseases and their potential therapeutic approaches.
Graphical abstract
The primary cause of free radical generation is drug overdosing, industrial air pollution, toxic heavy metals, ionizing radiation, smoking, alcohol, pesticides, and ultraviolet radiation. Excessive generation of free radicals inside the cell R1Q1 increases reactive oxygen and nitrogen species, which causes oxidative damage. An increase in oxidative damage alters different cellular pathways and processes such as mitochondrial impairment, DNA damage response, cell cycle arrest, and inflammatory response, leading to pathogenesis and progression of neurodegenerative disease other neurological defects.
