Ionoregulatory disruption as the acute toxic mechanism for lead in the rainbow trout (Oncorhynchus mykiss)

J. T. Rogers, J. G. Richards, C. M. Wood

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139 Scopus citations


The mechanism for acute toxicity of lead (Pb) in rainbow trout (Oncorhynchus mykiss) was investigated at Pb concentrations close to the 96 h LC50 of 1.0 mg dissolved Pb l-1 (0.8-1.4, 95% C.I.) determined in dechlorinated Hamilton city tap water (from Lake Ontario, hardness=140 mg l-1 CaCO3). Tissue Pb accumulation associated with death was highest in the gill, followed by kidney and liver. Significant ionoregulatory impacts were observed in adult rainbow trout (200-300 g) fitted with indwelling dorsal aortic catheters and exposed to 1.1±0.04 mg dissolved Pb l-1. Decreased plasma [Ca2+], [Na+] and [Cl-] occurred after 48 h of exposure through to 120 h, with increases in plasma [Mg2+], ammonia, and cortisol. No marked changes in PaO2, PaCO2, pH, glucose, or hematological parameters were evident. Branchial Na+/K+ ATPase activity in juvenile trout exposed to concentrations close to the 96 h LC50 was inhibited by approximately 40% after 48 h of Pb exposure. Calcium ion flux measurements using 45Ca as a radiotracer showed 65% inhibition of Ca2+ influx after 0, 12, 24 or 48 h exposure to the 96 h LC50 concentration of Pb. There was also significant inhibition (40-50%) of both Na+ and Cl- uptake, measured with 22Na and 36Cl simultaneously. We conclude that the mechanism of acute toxicity for Pb in rainbow trout occurs by ionoregulatory disruption rather than respiratory or acid/base distress at Pb concentrations close to the 96 h LC50 in moderately hard water.

Original languageEnglish (US)
Pages (from-to)215-234
Number of pages20
JournalAquatic Toxicology
Issue number2
StatePublished - Jul 16 2003


  • Acute toxicity
  • Ionoregulation
  • Lead
  • Rainbow trout
  • Waterborne

ASJC Scopus subject areas

  • Aquatic Science


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