Renal function in the freshwater rainbow trout (Oncorhynchus mykiss) following acute and prolonged exposure to waterborne nickel.

Renal function was investigated in adult rainbow trout following acute and prolonged exposure to waterborne Ni in moderately hard Lake Ontario water (approximately 140 mgL(-1) as CaCO3). Fish were exposed for 36 days to a sublethal concentration of 442 microg Ni L(-1), followed by 96 h of exposure to 12,850 microg 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 (P(i)), 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 UER(Mg2+) 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-HCO3), 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.