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Table 1.

Actual metal concentrations measured in the water of the exposure tanks.

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Table 1 Expand

Fig 1.

The four-parameter logistic fit of the model to the data set of copper, cadmium and zinc exposure for 240 hours.

Mortality is plotted as a function of the nominal concentration of the respective metal ion (in μM).

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Fig 1 Expand

Table 2.

Parameters used for the logistic function to plot the dose-response relationship for the 96h and 240h exposure experiment.

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Table 2 Expand

Fig 2.

The trend in lethal level for 50% of common carp juveniles ((LC50) for the three metals copper (a), cadmium (b) and zinc (c) tested over a time span of 10 days (240 hours).

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Fig 2 Expand

Fig 3.

Metal uptake rate (mean ± SEM) during the 240 hours toxicity screening test for the different exposure concentrations (in μM), for copper (a), cadmium (b) and zinc (c) exposure. The total metal content (in μg/g dry weight) measured in the whole body is corrected for the average value of the respective metal in the control fish. The y-axis expresses the uptake rate in hours of exposure with error bars as standard error of mean.

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Fig 4.

Total copper (a), cadmium (b) and zinc (c) accumulated in the gills expressed in micrograms per gram of dry weight (mean ± SEM). The metal content was measured after 1, 3 and 7 days of exposure for the 3 experimental groups; control (dark grey), low dose (light grey) and high dose (white). Day 0 refers to the time zero control group (black). Letters denote significant differences among treatments and within 1 sampling day, found with Dunn’s test of multiple comparisons (Bonferroni adjusted p-value rejects H0 if p< = 0.05/2).

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Fig 4 Expand

Table 3.

The results of the linear regression analysis to find associations between accumulated metals in the gills and electrolyte levels.

The slope and the Pearson correlation coefficient are provided with the corresponding p-value. Significant associations (p < 0.05) are highlighted in with “*”, N = 18.

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Table 3 Expand

Fig 5.

Micrographs of some of histopathological alterations found in the gills of common carp in the present study: a) normal tissue structure (H/E x200); b) note the extensive hyperemia on secondary lamellae (arrows; H/E x400); c) hypertrophy of squamous epithelial cells (arrows); compare thickness of these cells to non-pathological cell (arrowhead). Furthermore, note the size of the nuclei in both type of cells (H/E x1000); d) disturbed architecture of secondary lamellae: curling and fusion (arrowheads; H/E x100); e) oedema of primary filament (arrowheads; H/E x200); f) total rupture of epithelium leading to necrosis (arrows; H/E x400).

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Fig 5 Expand

Table 4.

Mean values of histopathological scores of common carp from experimental groups.

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Table 4 Expand