Acute waterborne nickel toxicity in the rainbow trout ( Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism

• Published in: Aquatic toxicology Vol. 63; no. 1; pp. 65 - 82
• Main Authors: Pane, E.F., Richards, J.G., Wood, C.M.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 17.03.2003; Elsevier Science
• Subjects: 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; Ontario; Canada, Ontario, Ontario L; 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
• DOI: 10.1016/S0166-445X(02)00131-5
• ISSN: 0166-445X

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.