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膳食蛋氨酸硒对慢性暴露期间虹鳟鱼(Oncorhynchus mykiss)组织中砷酸盐的积累和毒性的影响。

The effects of dietary selenomethionine on tissue-specific accumulation and toxicity of dietary arsenite in rainbow trout (Oncorhynchus mykiss) during chronic exposure.

机构信息

Department of Biology, University of Saskatchewan, Saskatoon, SK, Canada.

出版信息

Metallomics. 2019 Mar 20;11(3):643-655. doi: 10.1039/c8mt00309b.

DOI:10.1039/c8mt00309b
PMID:30762050
Abstract

The interactive effects of different doses of dietary selenium [as selenomethionine; 1.8 μg g-1 (control), 10 μg g-1 and 40 μg g-1 diet] on the toxicity of dietary arsenic [as arsenite (As3+); 80 μg As per g diet] were investigated in rainbow trout over an exposure period of 30 days. Fish fed with As3+ alone showed an increased hepatic lipid peroxidation (LPO) and a concomitant decline in cellular redox potential (determined as GSH:GSSG) in the liver tissue relative to the control fish. Interestingly, fish fed with low (10 μg g-1) or high (40 μg g-1) concentration of dietary selenomethionine in combination with As3+ showed an even higher degree of hepatic LPO and a further decrease in GSH : GSSG molar ratio relative to the fish treated with As3+ alone. Our study also revealed that exposure to dietary selenomethionine (both at low and high levels) resulted in significantly higher levels of arsenic in target tissues (liver, kidney, and muscle) relative to fish treated with As3+ alone. Similarly, the synchrotron-based X-ray fluorescence imaging analysis also suggested a dose-dependent increase in the co-localization of arsenic and selenium in the brain of fish co-treated with dietary As3+ and selenomethionine. These observations suggested that selenomethionine facilitated arsenic deposition in the brain and likely in other tissues, possibly via bio-complexation. Overall, our findings indicated that elevated dietary selenomethionine can increase the tissue-specific accumulation and toxicity of As3+ in fish during chronic dietary exposure.

摘要

在 30 天的暴露期内,研究了不同剂量的膳食硒(作为硒代蛋氨酸;1.8μg g-1(对照)、10μg g-1 和 40μg g-1 饮食)对膳食砷(作为亚砷酸盐(As3+);80μg As/g 饮食)毒性的交互作用。与对照组相比,单独喂食 As3+的鱼表现出肝脂质过氧化(LPO)增加,同时肝组织中的细胞氧化还原电位(用 GSH:GSSG 测定)下降。有趣的是,与单独用 As3+处理的鱼相比,低(10μg g-1)或高(40μg g-1)浓度的膳食硒代蛋氨酸与 As3+联合喂食的鱼表现出更高程度的肝 LPO 和 GSH:GSSG 摩尔比进一步下降。我们的研究还表明,暴露于膳食硒代蛋氨酸(低水平和高水平)会导致靶组织(肝、肾和肌肉)中砷的含量明显高于单独用 As3+处理的鱼。同样,基于同步加速器的 X 射线荧光成像分析也表明,在与膳食 As3+和硒代蛋氨酸共同处理的鱼的大脑中,砷和硒的共定位呈剂量依赖性增加。这些观察结果表明,硒代蛋氨酸促进了砷在大脑和其他组织中的沉积,可能是通过生物络合作用。总的来说,我们的研究结果表明,在慢性膳食暴露期间,膳食硒代蛋氨酸的增加会增加鱼类组织中 As3+的特异性积累和毒性。

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