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Morphological changes in gill mitochondria-rich cells in cultured Japanese eel Anguilla japonica acclimated to a wide range of environmental salinity

Morphological changes in gill mitochondria-rich (MR) cells were examined in cultured Japanese eel acclimated to deionized freshwater (DFW), freshwater (FW), 30%-diluted seawater (DSW), and seawater (SW). The gill Nasup(+)/Ksup(+)-ATPase activity was higher in SW-acclimated eel than in those acclimat...

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Published in:Fisheries science 2009-09, Vol.75 (5), p.1147-1156
Main Authors: Seo, M.Y.(Tokyo Univ. (Japan)), Lee, K,M, Kaneko, T
Format: Article
Language:English
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Summary:Morphological changes in gill mitochondria-rich (MR) cells were examined in cultured Japanese eel acclimated to deionized freshwater (DFW), freshwater (FW), 30%-diluted seawater (DSW), and seawater (SW). The gill Nasup(+)/Ksup(+)-ATPase activity was higher in SW-acclimated eel than in those acclimated to DFW, FW, and DSW. Immunocytochemical observations revealed that MR cells in the gill filaments were most developed in SW, whereas MR cells in the lamellae were preferentially observed in DFW, suggesting that filament and lamellar MR cells are responsible for ion secretion and absorption, respectively. In scanning electron microscopic observations, the apical membrane of lamellar MR cells appeared as a flat or slightly projecting disk with a mesh-like structure on its surface. In contrast, the apical membrane of filament MR cells showed a slightly concave surface. Whole-mount immunocytochemistry revealed that most MR cells showed cystic fibrosis transmembrane conductance regulator immunoreaction in their apical region in fish in DSW and SW, but not in those in DFW and FW, indicating that MR cells developed in DSW and SW function as an ion-secreting site. In addition to MR cells, distinct Nasup(+)/Ksup(+)-ATPase immunoreaction was observed in the outermost layer of gill epithelia, suggesting that pavement cells are an additional site of ion uptake in the gills.
ISSN:0919-9268
1444-2906
DOI:10.1007/s12562-009-0144-7