Acute waterborne nickel toxicity in the rainbow trout ( Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism
The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout ( Oncorhynchus mykiss) in moderately hard (∼140 mg l −1 as CaCO 3) Lake Ontario water, where the 96-h LC 50 for juvenile trout (1.5–3.5 g) was 15.3 mg (12.7–19.0, 95% C.L.) dissolved Ni l −1. No marked im...
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Published in | Aquatic toxicology Vol. 63; no. 1; pp. 65 - 82 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier B.V
17.03.2003
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (
Oncorhynchus mykiss) in moderately hard (∼140 mg l
−1 as CaCO
3) Lake Ontario water, where the 96-h LC
50 for juvenile trout (1.5–3.5 g) was 15.3 mg (12.7–19.0, 95% C.L.) dissolved Ni l
−1. No marked impact of Ni exposure on average unidirectional or net fluxes of Na
+, Cl
−, or Ca
2+ was observed in juvenile trout exposed for 48–60 h to 15.6 mg Ni l
−1 as NiSO
4. Furthermore, when adult rainbow trout (200–340 g) were fitted with indwelling dorsal aortic catheters and exposed for 117 h to 11.6 mg Ni l
−1 as NiSO
4, plasma ions (Na
+, Cl
−, Ca
2+, and Mg
2+) were all well conserved. However, mean arterial oxygen tension dropped gradually to ∼35% of control values. This drop in
P
aO
2
was accompanied by an acidosis primarily of respiratory origin.
P
aCO
2
rose to more than double control values with a concomitant drop in arterial pH of 0.15 units. Acute respiratory toxicity was further evidenced by a significant increase in hematocrit (Ht), and plasma lactate, and a significant decrease in spleen hemoglobin (Hb). Following 117 h of exposure to 11.6 mg Ni l
−1, the gill, intestine, plasma, kidney, stomach, and heart accumulated Ni significantly, with increases of 60, 34, 28, 11, 8, and 3-fold, respectively. Brain, white muscle, liver, and bile did not significantly accumulate Ni. Plasma Ni exhibited a remarkable linear increase with time to levels approximately 30-fold higher than controls. We conclude that in contrast to most other metals, Ni is primarily a respiratory, rather than an ionoregulatory, toxicant at exposure levels close to the 96-h LC
50. The implications of a waterborne metal as an acute respiratory toxicant (as opposed to ionoregulatory toxicants such as Cu, Ag, Cd, or Zn) with respect to toxicity modeling are discussed. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0166-445X 1879-1514 |
DOI: | 10.1016/S0166-445X(02)00131-5 |