Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism
Pane, E.F.; Richards, J.G.; Wood, C.M. (2003). Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism. Aquat. Toxicol. 63(1): 65-82. https://dx.doi.org/10.1016/S0166-445X(02)00131-5
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X; e-ISSN 1879-1514, more
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| Keywords |
Chemical elements > Metals > Transition elements > Heavy metals > Nickel
Fishes > Osteichthyes > Salmoniformes > Salmonidae > Salmo > Freshwater fishes > Rainbow trout
Properties > Biological properties > Toxicity
Respiration
Oncorhynchus mykiss (Walbaum, 1792) [WoRMS]
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| Authors | | Top |
- Pane, E.F., correspondent
- Richards, J.G.
- Wood, C.M.
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| Abstract |
The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynch mykiss) Lake Ontario water, where the 96-h LC50 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 Ca2+ was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l-1 as NiSO4. 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 NiSO4, plasma ions (Na+, Cl-, Ca2+, and Mg2+) were all well conserved. However, mean arterial oxygen tension dropped gradually to ~35% of control values. This drop in PaO2 was accompanied by an acidosis primarily of respiratory origin. PaCO2 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 LC50. 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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