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首页> 外文期刊>Aquatic Toxicology >Effects of chronic waterborne nickel exposure on growth, ion homeostasis, acid-base balance, and nickel uptake in the freshwater pulmonate snail, Lymnaea stagnalis.
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Effects of chronic waterborne nickel exposure on growth, ion homeostasis, acid-base balance, and nickel uptake in the freshwater pulmonate snail, Lymnaea stagnalis.

机译:长期暴露于水基镍对淡水肺蜗牛(Lymnaea stagnalis)的生长,离子稳态,酸碱平衡和镍吸收的影响。

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The freshwater pulmonate snail, Lymnaea stagnalis, is the most sensitive aquatic organism tested to date for Ni. We undertook a series of experiments to investigate the underlying mechanism(s) for this observed hypersensitivity. Consistent with previous experiments, juvenile snail growth in a 21-day exposure was reduced by 48% relative to the control when exposed to 1.3 micro g l-1 Ni (EC20 less than the lowest concentration tested). Ca2+ homeostasis was significantly disrupted by Ni exposure as demonstrated by reductions in net Ca2+ uptake, and reductions in Ca2+ concentrations in the hemolymph and soft tissues. We also observed reduced soft tissue [Mg2+]. Snails underwent a significant alkalosis with hemolymph pH increasing from 8.1 to 8.3 and hemolymph TCO2 increasing from 19 to 22 mM in control versus Ni-exposed snails, respectively. Unlike in previous studies with Co and Pb, snail feeding rates were found to be unaffected by Ni at the end of the exposure. Snails accumulated Ni in the soft tissue in a concentration-dependent manner, and Ni uptake experiments with 63Ni revealed a biphasic uptake profile - a saturable high affinity component at low exposure concentrations (36-189 nM) and a linear component at the high exposure concentrations (189-1897 nM). The high affinity transport system had an apparent Km of 89 nM Ni2+ and Vmax of 2.4 nmol g-1 h-1. This equates to a log K of 7.1, significantly higher than log K's (2.6-5.2) for any other aquatic organisms evaluated to date, which will have implications for Biotic Ligand Model development. Finally, pharmacological inhibitors that block Ca2+ uptake pathways in snails did not inhibit Ni uptake, suggesting that the uptake of Ni does not occur via Ca2+ uptake pathways. As with Cu and Pb, the exact mechanism for the significant disruption in Ca2+ homeostasis and reduction in juvenile snail growth remains unknown.
机译:淡水肺蜗牛,Lymnaea stagnalis,是迄今为止对镍最敏感的水生生物。我们进行了一系列实验,以研究这种超敏反应的潜在机制。与先前的实验一致,当暴露于1.3 micro gl -1 Ni(EC 20 少)时,与对照组相比,在21天暴露下的幼蜗牛生长减少了48%比测试的最低浓度)。 Ca 2 + 的体内稳态被镍暴露所破坏,这表现为净Ca 2 + 吸收的减少以及Ca 2 + 浓度的降低。血淋巴和软组织。我们还观察到软组织减少[Mg 2 + ]。与暴露于镍的蜗牛相比,对照的蜗牛经历了明显的碱中毒,血淋巴的pH值从8.1增加到8.3,血淋巴的TCO 2 从19mM增加到22mM。与以前对Co和Pb进行的研究不同,在暴露结束时,发现Ni不会影响蜗牛的摄食速度。蜗牛以浓度依赖的方式在软组织中积累Ni,而 63 Ni的Ni吸收实验显示出双相吸收曲线-在低暴露浓度(36-189 nM)和高暴露浓度(189-1897 nM)下的线性成分。高亲和力转运系统的表观K m 为89 nM Ni 2 + ,V max 为2.4 nmol g -1 < / sup> h -1 。这等于7.1的log K,大大高于迄今为止评估的任何其他水生生物的log K(2.6-5.2),这将对生物配体模型的开发产生影响。最后,阻断蜗牛中Ca 2 + 吸收途径的药理抑制剂不能抑制Ni的吸收,这表明Ni的吸收不是通过Ca 2 + 吸收途径发生的。与Cu和Pb一样,Ca 2 + 稳态显着破坏并降低幼蜗牛生长的确切机制仍不清楚。

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