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  • 1
    Keywords: Hochschulschrift
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (79 Seiten = 3,7 MB) , Illustrationen, Graphen, Karten
    Edition: 2021
    Language: English
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  • 2
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    In:  Supplement to: Holtmann, Wiebke C; Stumpp, Meike; Gutowska, Magdalena A; Syre, Stephanie; Himmerkus, Nina; Melzner, Frank; Bleich, Markus (2013): Maintenance of coelomic fluid pH in sea urchins exposed to elevated CO2: the role of body cavity epithelia and stereom dissolution. Marine Biology, 160(10), 2631-2645, https://doi.org/10.1007/s00227-013-2257-x
    Publication Date: 2023-02-24
    Description: Experimental ocean acidification leads to a shift in resource allocation and to an increased [HCO3-] within the perivisceral coelomic fluid (PCF) in the Baltic green sea urchin Strongylocentrotus droebachiensis. We investigated putative mechanisms of this pH compensation reaction by evaluating epithelial barrier function and the magnitude of skeleton (stereom) dissolution. In addition, we measured ossicle growth and skeletal stability. Ussing chamber measurements revealed that the intestine formed a barrier for HCO3- and was selective for cation diffusion. In contrast, the peritoneal epithelium was leaky and only formed a barrier for macromolecules. The ossicles of 6 week high CO2-acclimatised sea urchins revealed minor carbonate dissolution, reduced growth but unchanged stability. On the other hand, spines dissolved more severely and were more fragile following acclimatisation to high CO2. Our results indicate that epithelia lining the PCF space contribute to its acid–base regulation. The intestine prevents HCO3- diffusion and thus buffer leakage. In contrast, the leaky peritoneal epithelium allows buffer generation via carbonate dissolution from the surrounding skeletal ossicles. Long-term extracellular acid–base balance must be mediated by active processes, as sea urchins can maintain relatively high extracellular [HCO3-]. The intestinal epithelia are good candidate tissues for this active net import of HCO3- into the PCF. Spines appear to be more vulnerable to ocean acidification which might significantly impact resistance to predation pressure and thus influence fitness of this keystone species.
    Keywords: BIOACID; Biological Impacts of Ocean Acidification
    Type: Dataset
    Format: application/zip, 307.1 kBytes
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  • 3
    Publication Date: 2019-09-23
    Description: Experimental ocean acidification leads to a shift in resource allocation and to an increased [HCO3 −] within the perivisceral coelomic fluid (PCF) in the Baltic green sea urchin Strongylocentrotus droebachiensis. We investigated putative mechanisms of this pH compensation reaction by evaluating epithelial barrier function and the magnitude of skeleton (stereom) dissolution. In addition, we measured ossicle growth and skeletal stability. Ussing chamber measurements revealed that the intestine formed a barrier for HCO3 − and was selective for cation diffusion. In contrast, the peritoneal epithelium was leaky and only formed a barrier for macromolecules. The ossicles of 6 week high CO2-acclimatised sea urchins revealed minor carbonate dissolution, reduced growth but unchanged stability. On the other hand, spines dissolved more severely and were more fragile following acclimatisation to high CO2. Our results indicate that epithelia lining the PCF space contribute to its acid–base regulation. The intestine prevents HCO3 − diffusion and thus buffer leakage. In contrast, the leaky peritoneal epithelium allows buffer generation via carbonate dissolution from the surrounding skeletal ossicles. Long-term extracellular acid–base balance must be mediated by active processes, as sea urchins can maintain relatively high extracellular [HCO3 −]. The intestinal epithelia are good candidate tissues for this active net import of HCO3 − into the PCF. Spines appear to be more vulnerable to ocean acidification which might significantly impact resistance to predation pressure and thus influence fitness of this keystone species
    Type: Article , PeerReviewed
    Format: text
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