Failure of osmoregulation with apparent potassium intoxication in marine teleosts: A primary toxic effect of copper

Abstract Four sheepshead, Archosargus probatocephalus , weighing 665–980 g were exposed to toxic concentrations (8.5 p.p.m.) of cupric ion (copper) in sea water. Five stages of intoxication of increasing severity, based on behavior and posture, were designated as follows: lethargy; indifference; incoordination; moribundity; death. Serum, gills, liver, and kidneys were taken from fish at different stages of intoxication for examination. Kidneys were congested and swollen, the kidney wt/body wt index increasing up to 13.5 standard deviations (S.D.) over the mean control value. Gill lamellae from copper-poisoned fish were blunt and thickened, capillaries congested, and mucous cells dilated. Livers were similar to controls. Twenty-two clinical values were examined but only serum electrolytes and uric acid levels, liver and gill copper concentrations, kidney weights, and respiratory rates increased in poisoned fish by more than 5 S.D. over mean control values and correlated with the different stages of intoxication. Increased serum potassium, inorganic phosphate, and total intracellular ion values gave highest correlations with severity of intoxication. Potassium levels reached values considered lethal for mammals, and it was concluded that the intoxication following copper poisoning was a potassium intoxication caused primarily by cell damage and failure of osmoregulation by the gills and kidneys.