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    Publication Date: 2021-02-09
    Description: For finfish, coping with stress is not only relevant in the context of ecology but has also garnered lots of attention with respect to animal welfare in aquaculture. Yet, In particular the response to chronic stress still raises many questions regarding regulatory dynamics and mechanisms. I investigated the impact of two chronic stressors, relevant for aquaculture and ecology (hypercapnia and malnutrition), in two fish species, turbot (Psetta maxima) and Atlantic cod (Gadus morhua) via gene expression analysis. The aim of this study was to gain new insights in the respective coping mechanisms and detect potential communalities. Further, results were also screened for putative biomarkers for the detection and monitoring of environmental and culture induced stress. In each experiment, data pointed to divergent changes in gene expression between treatment levels, indicating different coping strategies dependent on the respective stress intensity. Further, my findings implied overall changes in lipid- and fatty acid metabolism as general part of the cellular response to chronic stress. Hints for additional hypoxia-like effects, reduced metabolic activity and increasing oxidative stress varied between the experiments, but seemed to increase parallel to the severity of the stressor. Several cues suggested that especially reactive oxygen species may play a central role in mediating both, regulation of gene expression and detrimental consequences of chronic stress. These findings provide new insights in the cellular response to chronic stress in fish and could help to improve contemporary stress and welfare concepts. The regulatory and damaging effects of reactive oxygen species provide a mechanistic explanation for divergent gene expression patterns and may also explain wear and tear like effects. Finally, I was able to identify multiple genes, which can be utilized as stress biomarkers in future studies.
    Type: Thesis , NonPeerReviewed
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  • 3
    Publication Date: 2022-01-31
    Description: Elevated concentrations of carbon dioxide are a common stressor for fish and other aquatic animals. In particular, intensive aquaculture can impose prolonged periods of severe environmental hypercapnia, manifold exceeding CO2 concentrations of natural habitats. In order to cope with this stressor, gills are essential and constitute the primary organ in the acclimatization process. Yet, despite a general understanding of changes in ion regulation, not much is known with regard to other cellular mechanisms. In this study, we apply RT-qPCR to investigate changes in the expression of several genes associated with metabolism, stress and immunity within gills of juvenile turbot (Psetta maxima) after an eight-week exposure to different concentrations of CO2 (low = ~3000 μatm, medium = ~15000 μatm and high = ~25000 μatm CO2). Histological examination of the gill tissue only found a significant increase of hypertrophied secondary lamella in the highest tested treatment level. gene expression results, on the other hand, implied both, mutual and dose-dependent transcriptional adjustments. Comparable up-regulation of IL-1ß, LMP7 and Grim19 at medium and high hypercapnia indicated an increase of reactive oxygen species (ROS) within gill cells. Simultaneous increase in Akirin and PRDX transcripts at medium CO2 indicated enhanced anti-oxidant activity and regulation of transcription, while reduced mRNA concentrations of COX, EF1α and STAT2 at high CO2 denoted suppressed protein synthesis and reduced metabolic capacity. In addition to upregulated DFAD and ApoE expression, implying compensating repair measures, gills exposed to the highest tested treatment level seemed to operate close to or even beyond their maximum capacity. Thus, fitting the model of capacity limitation, our results provide evidence for accretive intracellular hypoxia and oxidative stress in the gills of turbot, dependent on the level of environmental hypercapnia. Further, genes, such as COX, may be valuable biomarkers when attempting to discriminate between a successful and an overpowered stress response.
    Type: Article , PeerReviewed
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  • 4
    Publication Date: 2023-02-08
    Description: Highlights: • Larvae upregulate genes associated with fatty acid and glycogen synthesis under moderate ocean acidification (OA) • Larvae under high levels of OA fail to regulate • Dysfunctional metabolism and stress associated with pathologies in internal organs • Lack of differential gene regulation and stress response in juveniles correspond to a higher resilience to OA stress Elevated environmental carbon dioxide (pCO2) levels have been found to cause organ damage in the early life stages of different commercial fish species, including Atlantic cod (Gadus morhua). To illuminate the underlying mechanisms causing pathologies in the intestines, the kidney, the pancreas and the liver in response to elevated pCO2, we examined related gene expression patterns in Atlantic cod reared for two months under three different pCO2 regimes: 380 μatm (control), 1800 μatm (medium) and 4200 μatm (high). We extracted RNA from whole fish sampled during the larval (32 dph) and early juvenile stage (46 dph) for relative expression analysis of 18 different genes related to essential metabolic pathways. At 32 dph, larvae subjected to the medium treatment displayed an up-regulation of genes mainly associated with fatty acid and glycogen synthesis (GYS2, 6PGL, ACoA, CPTA1, FAS and PPAR1b). Larvae exposed to the high pCO2 treatment upregulated fewer but similar genes (6PGL, ACoA and PPAR1b,). These data suggest stress-induced alterations in the lipid and fatty acid metabolism and a disrupted lipid homeostasis in larvae, providing a mechanistic link to the findings of lipid droplet overload in the liver and organ pathologies. At 46 dph, no significant differences in gene expression were detected, confirming a higher resilience of juveniles in comparison to larvae when exposed to elevated pCO2 up to 4200 μatm.
    Type: Article , PeerReviewed , info:eu-repo/semantics/article
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