Physiological, molecular, and cellular mechanisms of impaired seawater tolerance following exposure of Atlantic salmon, Salmo salar, smolts to acid and aluminum.

摘要: We examined the physiological, molecular, and cellular mechanisms of impaired ion regulation in Atlantic salmon, Salmo salar, smolts following acute acid aluminum (Al) exposure. Smolts were exposed to: control (pH 6.5, 3.4 micrpg l(-1) Al), low Al (LAl: pH 5.4, 11 microg moderate (MAl: 5.3, 42 high (HAl: 56 Al) for two six days. At each time-point, sampled directly from freshwater treatment tanks after a 24h seawater challenge. Exposure to acid/MAl acid/HAl led accumulation gill Al, substantial alterations morphology, reduced Na(+)/K(+)-ATPase (NKA) activity, both seawater. days also decrease mRNA expression apical Cl(-) channel (cystic fibrosis transmembrane conductance regulator I), increased apoptosis upon exposure, an increase surface mitochondria-rich cells (MRCs) within filament epithelium gill, but abundance NKA-positive MRCs. By contrast, lowest concentration exhibited minor accumulation, slight morphological modifications tolerance absence detectable effect on regulation. These impacts accompanied by decreased cell proliferation, MRCs epithelium, no impact or total MRC was observed. However, gills acid/LAl including size, staining intensity, shape factor. demonstrate that salmon is extremely sensitive exposure levels underlying this depend time-course severity propose when are concentrations, results extensive damage transport protein abundance, synergistic stimulation When loss appears be independent these may result instead shift phenotype present epithelium.