Journal
AQUATIC TOXICOLOGY
Volume 72, Issue 1-2, Pages 119-133Publisher
ELSEVIER
DOI: 10.1016/j.aquatox.2004.11.020
Keywords
nickel; rainbow trout; renal physiology; prolonged exposure; acclimation
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Renal function was investigated in adult rainbow trout following acute and prolonged exposure to waterbome Ni in moderately hard Lake Ontario water (similar to 140 mg L-1 as CaCO3). Fish were exposed for 36 days to a sublethal concentration of 442 mu g Ni L-1, followed by 96 h of exposure to 12,850 mu g Ni L-1 (approximately 33% of the 96 h LC50). Prolonged exposure markedly affected only the renal handling of Ni, with no substantial effect on the plasma concentration, urinary excretion rate (UER) or clearance ratio (CR) of Na+, Cl-, K+, Ca2+, Mg2+, inorganic phosphate (Pi), glucose, lactate, total ammonia (T-amm), protein and free amino acids (FAA). Glomerular filtration rate (GFR) was reduced by 75% over 96 h of acute Ni challenge in both fish previously exposed to Ni and naive fish, with no significant change in urine flow rate (UFR), suggesting a substantial reduction in water reabsorption to maintain urine flow and water balance. Renal Mg2+ handling was specifically impaired by acute Ni challenge, leading to a significantly increased UERMg2+ and significantly decreased plasma [Mg2+] only in naive fish. Previously-exposed fish were well-protected against Ni-induced Mg2+ antagonism, indicating true acclimation to Ni. Only in naive, acutely challenged fish was there an increased UER of titratable acidity (TA-HCOA net acidic equivalents, P-i, T-amm and K+. Again, all of these parameters were well-conserved in previously-exposed fish during acute Ni exposure, strongly suggesting that prolonged, sublethal exposure protected against acute Ni-induced respiratory toxicity. (c) 2004 Elsevier B.V. All rights reserved.
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