TY - JOUR
T1 - Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism
AU - Pane, E. F.
AU - Richards, J. G.
AU - Wood, C. M.
PY - 2003/3/17
Y1 - 2003/3/17
N2 - 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 CaCO3) 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.
AB - 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 CaCO3) 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.
KW - Ionoregulation
KW - Nickel
KW - Rainbow trout
KW - Respiratory toxicity
KW - Waterborne
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U2 - 10.1016/S0166-445X(02)00131-5
DO - 10.1016/S0166-445X(02)00131-5
M3 - Article
C2 - 12615421
AN - SCOPUS:0037450933
VL - 63
SP - 65
EP - 82
JO - Aquatic Toxicology
JF - Aquatic Toxicology
SN - 0166-445X
IS - 1
ER -