Zoeken
Zoeken kan via de modus 'eenvoudig zoeken' (één veld) of uitgebreid via 'geavanceerd zoeken' (meerdere velden). Zo kan je bv. zoeken op een combinatie van een auteursnaam (auteur), een jaartal (jaar) en een documenttype.
Boekenmand
Nuttige resultaten kan je aanvinken en toevoegen aan een mandje. De inhoud hiervan kan je exporteren of afdrukken (naar bv. PDF).
RSS
Op de hoogte blijven van nieuw toegevoegde publicaties binnen uw interessegebied? Dit kan door een RSS-feed (?) te maken van jouw zoekopdracht.
nieuwe zoekopdracht
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
|  |
| Trefwoorden |
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]
|
| Auteurs | | Top |
- Pane, E.F., correspondent
- Richards, J.G.
- Wood, C.M.
|
|
|
| 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. |
IMIS is ontwikkeld en wordt gehost door het VLIZ.
