title: Acute waterborne nickel toxicity in the rainbow trout (Oncorhynchus mykiss) occurs by a respiratory rather than ionoregulatory mechanism.
abstract: 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.
authors.affiliation: Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ont., Canada L8S 4K1. paneef@mcmaster.ca
authors.forename: E F
authors.initials: EF
authors.lastname: Pane
authors.forename: J G
authors.initials: JG
authors.lastname: Richards
authors.forename: C M
authors.initials: CM
authors.lastname: Wood
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D018118:Chloride Channels / Q000187:drug effects; D004781:Environmental Exposure / Q000009:adverse effects*; D007928:Lethal Dose 50; D009532:Nickel / Q000633:toxicity*; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D009864:Ontario; D012137:Respiratory System / Q000187:drug effects*; D012964:Sodium / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D018118:Chloride Channels; D014874:Water Pollutants, Chemical; D009532:Nickel; D012964:Sodium; D002118:Calcium