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 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 P_aO2 was accompanied by an acidosis primarily of respiratory origin. P_aCO2 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.