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The mechanism of Pb-induced disruption of [Na.sup.+] and [Cl.sup.-] balance was investigated in the freshwater rainbow trout (Oncorhynchus mykiss). [Na.sup.+] and [Cl.sup.-] influx rates were reduced immediately in the presence of 2.40 [+ or -] 0.24 and 1.25 [+ or -] 0.14 [micro]M Pb, with a small increase in efflux rates occurring after 24-h exposure. Waterborne Pb caused a significant decrease in the maximal rate of [Na.sup.+] influx without a change in transporter affinity, suggesting a noncompetitive disruption of [Na.sup.+] uptake by Pb. Phenamil and bafilomycin markedly reduced [Na.sup.+] influx rate but did not affect Pb accumulation at the gill. Time-course analysis in rainbow trout exposed to 0, 0.48, 2.4, and 4.8 [micro]M Pb revealed time- and concentrationdependent branchial Pb accumulation. [Na.sup.+]-[K.sup.+]-ATPase activity was significantly reduced, with 4.8 [micro]M exposure resulting in immediate enzyme inhibition and 0.48 and 2.4 [micro]M exposures inhibiting activity by 24 h. Reduced activity was weakly correlated with gill Pb accumulation after 3- and 8-h exposures; this relationship strengthened by 24 h. Reduced [Na.sup.+] uptake was correlated with gill Pb burden after exposures of 3, 8, and 24 h. Immediate inhibition of branchial carbonic anhydrase activity occurred after 3-h exposure to 0.82 [+ or -] 0.05 or 4.30 [+ or -] 0.05 [micro]M Pb and continued for up to 24 h. We conclude that Pb-induced disruption of [Na.sup.+] and [Cl.sup.-] homeostasis is in part a result of rapid inhibition of carbonic anhydrase activity and of binding of Pb with [Na.sup.+]-[K.sup.+]-ATPase, causing noncompetitive inhibition of [Na.sup.+] and [Cl.sup.-] influx. waterborne lead; [Na.sup.+]-[K.sup.+]-ATPase; carbonic anhydrase; ionoregulation

The mechanism of Pb-induced disruption of Na+ and Cl- balance was investigated in the freshwater rainbow trout (Oncorhynchus mykiss). Na+ and Cl- influx rates were reduced immediately in the presence of 2.40 ± 0.24 and 1.25 ± 0.14 µM Pb, with a small increase in efflux rates occurring after 24-h exposure. Waterborne Pb caused a significant decrease in the maximal rate of Na+ influx without a change in transporter affinity, suggesting a noncompetitive disruption of Na+ uptake by Pb. Phenamil and bafilomycin markedly reduced Na+ influx rate but did not affect Pb accumulation at the gill. Time-course analysis in rainbow trout exposed to 0, 0.48, 2.4, and 4.8 µM Pb revealed time- and concentration-dependent bronchial Pb accumulation. Na+-K+-ATPase activity was significantly reduced, with 4.8 µM exposure resulting in immediate enzyme inhibition and 0.48 and 2.4 µM exposures inhibiting activity by 24 h. Reduced activity was weakly correlated with gill Pb accumulation after 3- and 8-h exposures; this relationship strengthened by 24 h. Reduced Na+ uptake was correlated with gill Pb burden after exposures of 3, 8, and 24 h. Immediate inhibition of branchial carbonic anhydrase activity occurred after 3-h exposure to 0.82 ± 0.05 or 4.30 ± 0.05 µM Pb and continued for up to 24 h. We conclude that Pb-induced disruption of Na+ and Cl- homeostasis is in part a result of rapid inhibition of carbonic anhydrase activity and of binding of Pb with Na+-K+-ATPase, causing noncompetitive inhibition of Na+ and Cl- influx. [ABSTRACT FROM AUTHOR]

We examined intraspecific variation in ionoregulatory physiology within euryhaline killifish, Fundulus heteroclitus, to understand possible mechanisms of freshwater adaptation in fish. Pronounced differences in freshwater tolerance existed between northern (2% mortality) and southern (19% mortality) killifish populations after transfer from brackish water (10 g 1-1) to freshwater. Differences in Na+ regulation between each population might partially account for this difference in tolerance, because plasma Na+ was decreased for a longer period in southern survivors than in northerns. Furthermore, northern fish increased Na+/K+-ATPase mRNA expression and activity in their gills to a greater extent 1–14 days after transfer than did southerns, which preceded higher whole-body net flux and unidirectional influx of Na+ at 14 days. All observed differences in Na+ regulation were small, however, and probably cannot account for the large differences in mortality. Differences in CI- regulation also existed between populations. Plasma CI- was maintained in northern fish, but in southerns, plasma CI- decreased rapidly and remained low for the duration of the experiment. Correspondingly, net CI- loss from southern fish remained high after transfer, while northerns eliminated CI- loss altogether. Elevated CI- loss from southern fish in freshwater was possibly due to a persistence of seawater gill morphology, as paracellular permeability (indicated by extrarenal clearance rate of PEG-4000) and apical crypt density in the gills (detected using scanning electron microscopy) were both higher than in northern fish. These large differences in the regulation of CI- balance probably contributed to the marked differences in mortality after freshwater transfer. Glomerular filtration rate and urination frequency were also lower in southerns. Taken together, these data suggest that northern killifish are better adapted to freshwater environments and that minimizing Cl- imbalance appears to be the key physiological difference accounting for their greater freshwater tolerance. [ABSTRACT FROM AUTHOR]