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Advisor(s)
Abstract(s)
A histopathological screening was performed on juvenile Senegalese soles exposed to
environmentally realistic concentrations of waterborne Cd (0.5, 5 and 10 lg L-1
) for 28 days. The
severity and dissemination of histopathological
changes were variable and limited to the kidney, liver,
spleen, gills and skin goblet cells. Contradicting
available literature that refers the liver as the most
affected organ upon acute exposure and the kidney
following chronic exposure, the liver was the most
impacted organ (even at the lowest concentration), in a
trend that could relate to the duration of exposure and
Cd concentration. The most noticeable hepatic alterations related to inflammation, although hepatocellular alterations like lipidosis and eosinophilic foci also occurred. The trunk kidney of exposed fish endured
moderate inflammation, apoptosis and necrosis, however, without a clear time-dependent effect. The
spleen of fish subjected to the highest concentrations
revealed diffuse necrotic foci accompanied by melanomacrophage intrusion. The gills, albeit the most
important apical uptake organ of dissolved toxicants,
sustained only moderate damage, from epithelial
hyperplasia and pavement cell detachment to the
potentially more severe chloride cell alterations. In the
skin, an increase in goblet cell size occurred, most
notoriously correlated to Cd concentration at earlier
stages of exposure. The results show that a metal-naı¨ve
juvenile fish can endure deleterious effects when
exposed to low, ecologically relevant, concentrations
of a common toxic metal and that the pattern of Cdinduced histopathological alterations can be complex
and linked to organ-specific responses and metal
translocation within the organism.
Description
Keywords
Histopathology Metal Solea senegalensis Sub-lethal exposure Bioassays