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铅导致虹鳟(Oncorhynchus mykiss)钠和氯平衡紊乱的潜在机制。

Mechanisms behind Pb-induced disruption of Na+ and Cl- balance in rainbow trout (Oncorhynchus mykiss).

作者信息

Rogers Joseph T, Patel Monika, Gilmour Kathleen M, Wood Chris M

机构信息

Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4K1, Canada.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2005 Aug;289(2):R463-R472. doi: 10.1152/ajpregu.00362.2004.

DOI:10.1152/ajpregu.00362.2004
PMID:16014449
Abstract

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 muM 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 microM Pb revealed time- and concentration-dependent branchial Pb accumulation. Na(+)-K(+)-ATPase activity was significantly reduced, with 4.8 microM exposure resulting in immediate enzyme inhibition and 0.48 and 2.4 microM 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 microM 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.

摘要

在淡水虹鳟(Oncorhynchus mykiss)中研究了铅诱导的钠(Na⁺)和氯(Cl⁻)平衡破坏机制。在存在2.40±0.24和1.25±0.14 μM铅的情况下,钠(Na⁺)和氯(Cl⁻)流入速率立即降低,暴露24小时后流出速率略有增加。水体中的铅导致钠(Na⁺)流入的最大速率显著降低,而转运体亲和力没有变化,这表明铅对钠(Na⁺)摄取有非竞争性破坏作用。非那明和巴弗洛霉素显著降低了钠(Na⁺)流入速率,但不影响鳃中铅的积累。对暴露于0、0.48、2.4和4.8 μM铅的虹鳟进行的时间进程分析显示,鳃中铅的积累具有时间和浓度依赖性。钠钾ATP酶(Na⁺-K⁺-ATPase)活性显著降低,暴露于4.8 μM导致酶立即受到抑制,暴露于0.48和2.4 μM在24小时后抑制活性。暴露3小时和8小时后,活性降低与鳃中铅的积累弱相关;这种关系在24小时时增强。暴露3小时、8小时和24小时后,钠(Na⁺)摄取减少与鳃中铅负荷相关。暴露于0.82±0.05或4.30±0.05 μM铅3小时后,鳃碳酸酐酶活性立即受到抑制,并持续长达24小时。我们得出结论,铅诱导的钠(Na⁺)和氯(Cl⁻)稳态破坏部分是由于碳酸酐酶活性的快速抑制以及铅与钠钾ATP酶(Na⁺-K⁺-ATPase)结合,导致对钠(Na⁺)和氯(Cl⁻)流入的非竞争性抑制。

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