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首页> 外文期刊>American Journal of Physiology >Time course analysis of the mechanism by which silver inhibits active Na+ and Cl- uptake in gills of rainbow trout.
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Time course analysis of the mechanism by which silver inhibits active Na+ and Cl- uptake in gills of rainbow trout.

机译：对银抑制虹鳟active中活性Na +和Cl-吸收的机理进行时程分析。

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摘要

A time course analysis using (110m)Ag, (24)Na(+), and (36)Cl(-) examined gill silver accumulation and the mechanism by which waterborne silver (4.0 x 10(-8) M; 4.3 microg/l) inhibits Na(+) and Cl(-) uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na(+), and Cl(-). To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na(+) and Cl(-) uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na(+) and Cl(-) uptake declined simultaneously and equally initially, with both uptakes reduced by approximately 500 nmol.g(-1).h(-1) over the 1st h of silver exposure. There was a further progressive decline in Na(+) uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na(+)-K(+)-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na(+) and Cl(-) uptake, whereas the later decline is probably related to Na(+)-K(+)-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na(+) and Cl(-) uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.
机译：使用（110m）Ag，（24）Na（+）和（36）Cl（-）进行时程分析，研究了g银的积累以及水性银（4.0 x 10（-8）M; 4.3 microg / l）抑制淡水虹鳟g中Na（+）和Cl（-）的吸收。通过对g和体通量的分析，可以计算出银，Na（+）和Cl（-）的根吸收率和基底外侧出口率。为了避免银生物利用度的变化，使用流通条件来限制暴露水中有机物的积累。对于Na（+）和Cl（-）的吸收，限速步骤是顶端进入而不是基底外侧出口。 Na（+）和Cl（-）的吸收同时开始且均等地下降，在银暴露的第一小时内，两者的吸收均减少了约500 nmol.g（-1）.h（-1）。直到24小时，Na（+）的摄入量进一步下降。碳酸酐酶活性被抑制1 h，而Na（+）-K（+）-ATPase活性直到暴露24 h才被显着抑制。这些结果表明碳酸酐酶抑制可以解释Na（+）和Cl（-）吸收的早期下降，而后来的下降可能与Na（+）-K（+）-ATPase的阻断有关。与以前的报道相反，g银的积累稳定地增加到了一个平台。尽管快速抑制了根尖Na（+）和Cl（-）的吸收，但根尖银的吸收（和基底外侧输出）一直增加到10小时，之后才减少。因此，短期内银不会抑制其自身的顶端吸收。这些结果表明，降低的银生物利用度是先前报道的静态暴露于银时g银积累峰值和下降模式背后的机制。

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