Bioaccumulation, distribution and retention of 63Ni2+ in the Brown trout (Salmo trutta)

Tjälve, Hans; Gottofrey, James; Borg, Kathleen

doi:10.1016/0043-1354(88)90007-3

Cited by 26 publications

(7 citation statements)

References 12 publications

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“…Results of the present study indicate that brown trout readily bioaccumulate Mn(I1) from water when exposed to a low concentration for short periods. After a 1-week expo-sure under similar experimental conditions, brown trout accumulated three times less nickel [15], but nearly seven times more mercury [ 161 and 11 times more cadmium [ 171 than Mn as found in the current study. After 6 weeks of exposure to Mn, the whole body BCF was 17.8.…”

Section: Uptake and Depurationsupporting

confidence: 79%

UPTAKE, DISTRIBUTION AND ELIMINATION OF 54Mn(II) IN THE BROWN TROUT (SALMO TRUTTA)

Rouleau¹,

Tjälve²,

Gottofrey³

et al. 1995

Environ Toxicol Chem

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Brown trout (Salmo frutfa) were exposed to water containing 0.1 pg.L-' (1.8 nmo1.L-I) of s4Mn(Il) for 1, 3, or 6 weeks. Additional trout were exposed for 3 weeks and allowed to depurate for 1 or 3 weeks. Both the uptake and the organ distribution of manganese (Mn) were determined by gamma counting and whole-body autoradiography. Steady-state concentration, C,,, and biological half-life, f,,,, were calculated. The whole-body Mn concentration (1.78 pg.kg-l) reached after 6 weeks o f exposure was close to C,, (1.88 pg.kg-') and f,,, was 9.6 d. Manganese concentration in tissues followed the decreasing order liver > viscera without liver and kidney > gills > skin, fins, bones, and head excluding gills, brain, and eyes > kidney = epidermal mucus > brain > eyes > muscle. Autoradiograms indicated high Mn concentrations in the pancreatic tissue, skeleton, gastrointestinal mucosa, and olfactory system. Gills, viscera, and eyes (tl,2 = 3.7 to 8.8 d) were near steady state after 6 weeks of exposure, while the other tissues were not ( t l I 2 = 14.6 to 26.4 d). The depuration rate of total radioactivity was relatively rapid initially as 22% of Mn content was lost during the first week, and became slower in the following 2 weeks. Participation of Mn in enzymatic activities of liver, pancreas, and gastrointestinal mucosa may explain its high uptake in these tissues, whereas accumulation in the skeleton seems to be related to bone formation. The uptake of Mn by way of olfactory system favoured its accumulation in the brain of trout. As Mn is known to be neurotoxic, we suggest this route of uptake could be of toxicological significance for fish.

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Section: Uptake and Depurationsupporting

confidence: 79%

UPTAKE, DISTRIBUTION AND ELIMINATION OF 54Mn(II) IN THE BROWN TROUT (SALMO TRUTTA)

Rouleau¹,

Tjälve²,

Gottofrey³

et al. 1995

Environ Toxicol Chem

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“…As summarized above, the available data for these organisms suggest that nickel may be actively regulated. Alikhan and Zia (1989) directly measured what appears to be active uptake and excretion of nickel in the crayfish Cambarus bartoni, while nickel concentrations in the kidney of fish, a common organ for excretion of metals, appear to contain proportionally more nickel than other organs (Ray et al 1990;Tjalve et al 1988). These data support the idea that the inverse relationships observed between BCF and water concentration for crustaceans and fish ( Figs.…”

Section: Nickel Tissue Distribution Datasupporting

confidence: 64%

“…Accordingly, the data from Ray et al (1990) suggest the catfish may be eliminating excess nickel via the kidney. Tjalve et al (1988) exposed brown trout (Salmo trutta) to nickel concentrations of 0.1 and 10 µg/L (within reasonable background levels for nickel) for 7 d and, like Ray et al (1990), the highest proportion of nickel concentrations were measured in the kidney.…”

Section: Nickel Tissue Distribution Datamentioning

confidence: 77%

Nickel essentiality and homeostasis in aquatic organisms

Muyssen¹,

Brix²,

DeForest³

et al. 2004

Environ. Rev.

108

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It has been well established that a number of trace metals are essential for various biological functions and are critical in many of the enzymatic and metabolic reactions occurring within an organism. The essentiality of nickel is now generally accepted, based on the numerous symptoms caused by nickel deficiency (mainly in terrestrial vertebrates) and its essential role in various enzymes in bacteria and plants. The information on optimal and deficient concentrations of nickel, however, is limited and the essentiality of nickel to aquatic animals is not established. The purpose of this review is to synthesize the available information on nickel essentiality and homeostasis in aquatic organisms. There is less information on these topics compared to that for other essential metals. Nickel essentiality to aquatic organisms can only be confirmed for plants and (cyano)bacteria due to the documented role of nickel in the urease and hydrogenase metabolism. Deficiency levels ranged from 10-12 M to 2 × 10-6 M Ni in different species. No studies were identified that had the explicit objective of evaluating homeostatic mechanisms for nickel in aquatic life. However, inferences could be made through the evaluation of nickel bioconcentration and tissue distribution data and a comparison to other metals that have been more thoroughly studied. Data suggest active regulation and therefore nickel essentiality, since there are no known examples of active regulation of non-essential metals in invertebrates. Key words: nickel, essentiality, homeostasis, bioconcentration, regulation.

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“…For example, nickel residues in the kidney of the shark Galeus melastamus collected from the coast of Scotland averaged only 1.61 mg/kg, essentially similar to that observed for muscle (Table 17.9). Tjalve et al (1988) exposed brown trout Salrna truUa to water containing 0.1 or 10 /Lg/L of 63Ni2+. After 3 weeks of exposure, the whole body concentration of nickel was about eight times greater than that of water.…”

Section: Fishmentioning

confidence: 99%

“…"One group of fish was exposed to Ni prior to analysis whereas the second group of fish was allowed to swim in postexposure Ni-free water prior to analysis. Source: Tjalve et al (1988).…”

Section: Toxic Effects To Aquatic Organismsmentioning

confidence: 99%