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 | |
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Abstract | 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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AbstractList | Juvenile rainbow trout were exposed to water from Lake Ontario containing various concentrations of dissolved nickel to determine the 96-hour LC super(50), which was calculated at 15.3 mg/l. Exposure of juveniles for up to 60 hours in water containing 15.6 mg Ni/l did not adversely affect sodium, chloride, or calcium ion flux. Aortic catheterization of adult fish prior to exposure to 11.6 mg Ni for 117 h showed conservation of plasma ions, but a gradual decline in oxygen tension in the arteries, and increasing respiratory acidosis that was confirmed by elevations in plasma lactate levels and hematocrit and a reduction in hemoglobin levels in the spleen. Significant bioaccumulation of Ni was demonstrated in gill, plasma, intestine, heart, stomach, and kidney, without any such increases in Ni content of brain, liver, bile, or muscle. Bioaccumulation increased linearly with duration of exposure. The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( approximately 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 approximately 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. The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( similar to 140 mg l super(-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 super(-1). No marked impact of Ni exposure on average unidirectional or net fluxes of Na super(+), Cl super(-), or Ca super(2+) was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l super(-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 super(-1) as NiSO4, plasma ions (Na super(+), Cl super(-), Ca super(2+), and Mg super(2+)) were all well conserved. However, mean arterial oxygen tension dropped gradually to similar 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 super(-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. The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard (~140 mg l super(-1) as CaCO sub(3)) Lake Ontario water, where the 96-h LC sub(50) for juvenile trout (1.5-3.5 g) was 15.3 mg (12.7-19.0, 95% C.L.) dissolved Ni l super(-1). No marked impact of Ni exposure on average unidirectional or net fluxes of Na super(+), Cl super(-), or Ca super(2+) was observed in juvenile trout exposed for 48-60 h to 15.6 mg Ni l super(-1) as NiSO sub(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 super(-1) as NiSO sub(4), plasma ions (Na super(+), Cl super(-), Ca super(2+), and Mg super(2+)) were all well conserved. However, mean arterial oxygen tension dropped gradually to ~35% of control values. This drop in PaO sub(2) was accompanied by an acidosis primarily of respiratory origin. PaCO sub(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 super(-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 sub(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. 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. |
Author | Pane, E.F. Richards, J.G. Wood, C.M. |
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Keywords | Respiratory toxicity Nickel Ionoregulation Rainbow trout Waterborne Salmonidae Ionic regulation Toxicity Exposure Oncorhynchus mykiss Heavy metal Freshwater environment Vertebrata Lethal dose 50 Pisces Water pollution Biological accumulation Mechanism of action Respiration |
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Snippet | 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... The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( approximately 140 mg... Juvenile rainbow trout were exposed to water from Lake Ontario containing various concentrations of dissolved nickel to determine the 96-hour LC super(50),... The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard ( similar to 140 mg l... The acute mechanism of toxicity of waterborne nickel (Ni) was investigated in the rainbow trout (Oncorhynchus mykiss) in moderately hard (~140 mg l super(-1)... |
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SubjectTerms | Acid-Base Equilibrium - drug effects Agnatha. Pisces Animal, plant and microbial ecology Animals Applied ecology Biological and medical sciences Calcium - metabolism Chloride Channels - drug effects Ecotoxicology, biological effects of pollution Effects of pollution and side effects of pesticides on protozoa and invertebrates Effects of pollution and side effects of pesticides on vertebrates Environmental Exposure - adverse effects Freshwater Fundamental and applied biological sciences. Psychology Ionoregulation Lethal Dose 50 Nickel Nickel - toxicity Oncorhynchus mykiss Oncorhynchus mykiss - metabolism Ontario Rainbow trout Respiratory System - drug effects Respiratory toxicity Sodium - metabolism Water Pollutants, Chemical - toxicity Waterborne |
Title | Acute waterborne nickel toxicity in the rainbow trout ( Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism |
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