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虹鳟(Oncorhynchus mykiss)离体灌注肠道对无机汞的剂量依赖性吸收涉及氨氯地平敏感途径和能量依赖途径。

Dose-dependent inorganic mercury absorption by isolated perfused intestine of rainbow trout, Oncorhynchus mykiss, involves both amiloride-sensitive and energy-dependent pathways.

作者信息

Hoyle I, Handy R D

机构信息

School of Biological Sciences, University of Plymouth, Drake Circus, Plymouth PL4 8AA, UK.

出版信息

Aquat Toxicol. 2005 Mar 25;72(1-2):147-59. doi: 10.1016/j.aquatox.2004.11.015.

Abstract

The trophic transfer and nutritional toxicity of mercury (Hg) in aquatic food chains is well known, but there is limited information on the mechanism of mercury uptake across the gut. In this study, isolated whole gut sacs from rainbow trout were used to identify the regions of the gut involved in Hg absorption, and then perfused intestines were used to investigate Hg uptake. Exposure of whole gut sacs to 100 micromol l(-1) Hg as HgCl2 in the luminal solution caused Hg accumulation primarily in the mucosa (78% or more), with the intact mid and hind gut supporting 59% of the accumulated Hg. Luminal exposure to [Hg] between 0 and 100 micromol l(-1) for 4 h in perfused trout intestines showed a non-linear dose-dependent accumulation with a maximum Hg uptake rate of about 103 nmol g(-1) h(-1), and suggests carrier mediated transport into the gut cells and the blood. Additions of 2 mmol l(-1) amiloride depressed Hg accumulation by the mid and hind gut by 40-50%, whilst additions of the Ca chelator 1 mmol l(-1) EGTA increased Hg levels in the tissue. Symmetrical additions of 10 mmol l(-1) cyanide did not prevent tissue accumulation of Hg, but caused a 3.4-fold decline in net Hg flux to the serosal compartment. We conclude that Hg absorption across the gut is partly carrier mediated and involves both amiloride sensitive, and energy-dependent pathways.

摘要

汞(Hg)在水生食物链中的营养转移和营养毒性是众所周知的,但关于汞跨肠道吸收机制的信息有限。在本研究中,使用虹鳟鱼分离的全肠囊来确定肠道中参与汞吸收的区域,然后使用灌注肠来研究汞的吸收。将全肠囊暴露于管腔溶液中100 μmol l⁻¹的HgCl₂形式的汞,导致汞主要在黏膜中积累(78%或更多),完整的中肠和后肠支持了59%的积累汞。在灌注的鳟鱼肠道中,将管腔暴露于0至100 μmol l⁻¹的[Hg]中4小时,显示出非线性剂量依赖性积累,最大汞吸收速率约为103 nmol g⁻¹ h⁻¹,这表明存在载体介导的转运进入肠道细胞和血液。添加2 mmol l⁻¹的氨氯吡咪使中肠和后肠的汞积累降低了40 - 50%,而添加1 mmol l⁻¹的钙螯合剂乙二醇双四乙酸(EGTA)则增加了组织中的汞水平。对称添加10 mmol l⁻¹的氰化物并不能阻止组织中汞的积累,但导致向浆膜腔的净汞通量下降了3.4倍。我们得出结论,汞跨肠道的吸收部分是由载体介导的,涉及氨氯吡咪敏感和能量依赖途径。

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