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Environmental fate & pathways

Additional information on environmental fate and behaviour

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Endpoint:
additional information on environmental fate and behaviour
Type of information:
experimental study
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Study meets generally accepted scientific methods and is described in sufficient detail.
Cross-referenceopen allclose all
Reason / purpose:
reference to same study
Reason / purpose:
reference to other study

Data source

Reference
Reference Type:
publication
Title:
Critical body residues, Michaelis-Menten analysis of bioaccumulation, lethality and behaviour as endpoints of waterborne Ni toxicity in two teleosts.
Author:
Leonard EM, Marentette JR, Balshine S, Wood CM.
Year:
2014
Bibliographic source:
Ecotoxicology. 2014 Mar;23(2):147-62. doi: 10.1007/s10646-013-1159-5. Epub 2014 Jan 9.

Materials and methods

Test guideline
Qualifier:
no guideline followed
Principles of method if other than guideline:
Kinetics were measured for two fish species
GLP compliance:
no
Type of study / information:
Kinetics

Test material

Reference
Name:
Unnamed
Type:
Constituent
Test material form:
other: stock solutions
Details on test material:
- Name of test material (as cited in study report): NiCl2.6H2O

Results and discussion

Any other information on results incl. tables

Ni bioaccumulation and Michaelis-Menten parameters

Prior to Ni exposure in the laboratory, the gills, gut, carcass and whole fish of round goby had 1.2-2.6x more Ni in comparison to trout, however, the liver and brain of rainbow trout had 2.1 and 3.8x more Ni, respectively, than the round goby. There was no significant difference in the kidney Ni level. In general, as the Ni exposure concentration increased so did Ni bioaccumulation (this was true for all organs and for both species apart from trout carcass/muscle). Ni bioaccumulation in organs and whole

fish (all organs combined) were comparable between the two species on a per weight basis (Fig. l). Primarily, Ni bioaccumulation occurred in the gills, kidney and gut, with less Ni in the guts of rainbow trout than round goby. Interestingly, little Ni was detected in the brain, suggesting that the blood-brain barrier is fairly efficient for this important behavioural control center. In round goby brains,

elevated Ni were observed only at the highest exposure concentration tested (221.3 umol Ni/L), while in rainbow trout brains, Ni bioaccumulation never exceeded the levels observed in the control fish.

Michaelis-Menten kinetic constants (Bmax and ~) for saturable Michaelis-Menten kinetic constants (Bmax and Kd) for saturable Ni bioaccumulation in the gill, gut, kidney and whole fish of round goby and rainbow trout  

 

Bmax(µmol/kg wet wt)

Kd(µmol Ni/L)

r2

Goby

 

 

 

  Gill

303.9a

17.8a

0.87

  Gut

509.4a

242.6a

0.99

  Kidney

396.2a

107.8a

0.97

  Whole fish

275.5a

539.6a

0.85

Trout

 

 

 

  Gill

277.6a

86.4a,c

0.99

  Gut

67.7b,c

75.3a,c

0.94

  Kidney

512.1c

211.2a

0.97

  Whole fish

19.5b

46.5a

0.91

The Bmax and ~ values were not calculated for the liver in either species and the carcass for round goby as the relationship between Ni exposure concentration and organ Ni bioaccumu1ation was linear. As well, in the brain and carcass of trout, no relationship was found between Ni exposure and organ Ni concentration.

Values are mean ± SEM

a.b Significant difference between Bmax and Kd values within a species

c Significant difference between a Bmax and Kd values of an organ or whole fish between the two species

Applicant's summary and conclusion

Executive summary:

STUDY RATED BY AN INDEPENDENT REVIEWER