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Effects of salinity on short-term waterborne zinc uptake, accumulation and sub-lethal toxicity in the green shore crab (Carcinus maenas)

机译:盐度对绿岸蟹(Carcinus maenas)短期水载锌摄入,积累和亚致死毒性的影响

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Waterborne zinc (Zn) is known to cause toxicity to freshwater animals primarily by disrupting calcium (Ca) homeostasis during acute exposure, but its effects in marine and estuarine animals are not well characterized. The present study investigated the effects of salinity on short-term Zn accumulation and sub-lethal toxicity in the euryhaline green shore crab, Carcinus maenas. The kinetic and pharmacological properties of short-term branchial Zn uptake were also examined. Green crabs (n = 10) were exposed to control (no added Zn) and 50 M (3.25 mg L-1) of waterborne Zn (similar to 25% of 96 h LC50 in 100 seawater) for 96 h at 3 different salinity regimes (100%, 60% and 20% seawater). Exposure to waterborne Zn increased tissue-specific Zn accumulation across different salinities. However, the maximum accumulation occurred in 20% seawater and no difference was recorded between 60% and 100% seawater. Gills appeared to be the primary site of Zn accumulation, since the accumulation was significantly higher in the gills relative to the hepatopancreas, haemolymph and muscle. Waterborne Zn exposure induced a slight increase in haemolymph osmolality and chloride levels irrespective of salinity. In contrast, Zn exposure elicited marked increases in both haemolymph and gill Ca levels, and these changes were more pronounced in 20% seawater relative to that in 60% or 100% seawater. An in vitro gill perfusion technique was used to examine the characteristics of short-term (1-4h) branchial Zn uptake over an exposure concentration range of 3-12 mu M (200-800 mu g L-1). The rate of short-term branchial Zn uptake did not change significantly after 2 h, and no difference was recorded in the rate of uptake between the anterior (respiratory) and posterior (ion transporting) gills. The in vitro branchial Zn uptake occurred in a concentration-dependent manner across different salinities. However, the rate of uptake was consistently higher in 20% seawater relative to 60% or 100% seawater - similar to the trend observed with tissue Zn accumulation during in vivo exposure. The short-term branchial Zn uptake was found to be inhibited by lanthanum (a blocker of voltage -independent Ca channels), suggesting that branchial Zn uptake occurs via the Ca transporting pathways, at least in part. Overall, our findings indicate that acute exposure to waterborne Zn leads to the disruption of Zn and Ca homeostasis in green crab, and these effects are exacerbated at the lower salinity. (C) 2016 Elsevier B.V. All rights reserved.
机译:众所周知,水基锌(Zn)会通过在急性暴露期间破坏钙(Ca)稳态而对淡水动物产生毒性,但对海洋和河口动物的作用尚不十分清楚。本研究调查了盐度对在淡水绿岸蟹Carcinus maenas中短期Zn积累和亚致死毒性的影响。还研究了短期分支锌吸收的动力学和药理特性。将青蟹(n = 10)在3种不同的盐度条件下暴露于对照(未添加锌)和50 M(3.25 mg L-1)的水基Zn(类似于100%海水中96 h LC50的25%)96小时。 (100%,60%和20%的海水)。暴露于水性锌会增加不同盐度下组织特异性锌的积累。但是,最大积累发生在20%的海水中,而60%和100%的海水之间没有差异。 appeared似乎是锌积累的主要部位,因为relative中的积累明显高于肝胰腺,血淋巴和肌肉。无论盐度如何,暴露于水中的锌都会导致血淋巴渗透压和氯化物含量略有增加。相反,锌的暴露引起血淋巴和and Ca含量显着增加,与60%或100%海水相比,这些变化在20%海水中更为明显。体外g灌流技术用于检查在3-12μM(200-800μg L-1)的暴露浓度范围内短期(1-4h)分支锌吸收的特征。 2 h后短期分支锌的吸收速率没有显着变化,并且前((呼吸道)和后g(离子转运)之间的吸收率没有差异。在不同盐度下,体外分支锌的吸收呈浓度依赖性。然而,相对于60%或100%海水,在20%海水中的摄取率一直较高-与体内暴露期间组织Zn积累所观察到的趋势相似。发现镧(一种与电压无关的Ca通道的阻滞剂)抑制了短期分支Zn的吸收,这表明分支Zn的吸收至少部分地通过Ca的运输途径发生。总体而言,我们的研究结果表明,急性接触水性锌会导致青蟹体内Zn和Ca稳态的破坏,而盐度较低时,这些影响会加剧。 (C)2016 Elsevier B.V.保留所有权利。

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