Modulating effects of dietary fats on methylmercury toxicity and distribution in rats
Modulating effects of dietary fats on methylmercury toxicity and distribution in rats
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DOI：
10.1016/j.tox.2006.10.023
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发表时间：
2007-01-25
期刊：
影响因子：
4.5
通讯作者：
Chan, Hing Man
中科院分区：
文献类型：
--
作者：
Jin, Xiaolei;Lok, Eric;Chan, Hing Man
食用鱼类是人类接触甲基汞的最重要来源。由于鱼类也是n - 3多不饱和脂肪酸的丰富来源，因此本研究旨在检查膳食脂肪对甲基汞诱导的大鼠急性毒性的影响。给断乳雄性Sprague道利大鼠喂食含大豆油、海豹油、二十二碳六烯酸（DHA）、鱼油或猪油的半纯化酪蛋白等热量饮食28天。然后每天对大鼠灌胃0、1或3毫克甲基汞/千克体重，连续14天喂食相同的食物。在实验的第43天，处死大鼠，收集血液样品并进行血液学分析。取出肝脏和脾脏，固定，并检查病理变化。分析血液、粪便、肝脏和大脑中的总汞和/或甲基汞含量。分析血清样本的肝损伤和免疫球蛋白的临床标志物。各组织中总汞含量随剂量的增加而增加。粪汞排泄量随甲基汞处理剂量和持续时间的增加而增加。饮食和甲基汞都表现出显着的影响，并相互作用显着的许多毒理学终点测量。甲基汞的许多影响取决于饮食。例如，在喂食猪油的大鼠中，与溶剂对照组相比，3毫克甲基汞/千克体重显著增加了肝脏和脾脏的相对重量;而在喂食鱼油、豆油、海豹油或DHA的大鼠中，甲基汞的这种影响不太明显或不存在，表明这些饮食具有保护作用。甲基汞在3毫克/公斤体重显着降低血清白蛋白水平，除DHA饮食组，这意味着保护DHA饮食对这一参数。只有在猪油饮食组，3毫克甲基汞/公斤体重显着增加血清胆红素水平，表明这种饮食对甲基汞毒性的增强作用。甲基汞抑制大鼠的适应性免疫系统，并以饮食依赖的方式刺激先天免疫系统。海豹油饮食提供了更强的抵抗力，而鱼油饮食使免疫系统对甲基汞的这些影响更敏感。这些结果意味着膳食脂肪对甲基汞毒性的调节作用很大，可能会转化为更严重或保护性的临床结果。因此，膳食脂肪是甲基汞暴露风险评估中需要考虑的重要因素。皇冠版权所有（c）2006出版的爱思唯尔爱尔兰有限公司保留所有权利。
Fish consumption is the most important source of human exposure to methyltuercury (MeHg). Since fish is also a rich source of n - 3 polyunsaturated fatty acids, this study was conducted to examine the effects of dietary fats on MeHg-induced acute toxicity in rats. Weanling male Sprague Dawley rats were administered semi-purified casein-based isocaloric diet containing soy oil, seal oil, docosahexaenoic acid (DHA), fish oil, or lard for 28 days. Rats were then gavaged with 0, 1, or 3 mg MeHg/kg body weight (BW) per day and fed the same diet for 14 consecutive days. On 43rd day of the experiment, rats were sacrificed and blood samples were collected and analyzed for hematology. Liver and spleen were removed, fixed, and examined for pathological changes. Blood, feces, liver, and brain were analyzed for total mercury and/or MeHg contents. Serum samples were analyzed for clinical markers of hepatic injury and immunoglobulin. Total mercury contents in all tissues measured increased with dose. Mercury excretion in feces increased with dose and duration of MeHg treatment. Both diets and MeHg showed significant effects and interacted significantly on many of the toxicological endpoints measured. Many of the effects of MeHg were diet-dependent. For example, in the rats fed the lard diet, 3 mg MeHg/kg BW significantly increased relative liver and spleen weight as compared with vehicle control; whereas in rats fed the fish oil, soy oil, seal oil, or DHA, this effect of MeHg was less obvious or absent, suggesting a protective effect of these diets. MeHg at 3 mg/kg BW significantly decreased serum albumin level in all except DHA dietary groups, implying a protection by the DHA diet on this parameter. Only in the lard dietary group, did 3 mg MeHg/kg BW significantly increase serum bilirubin level, indicating an enhancing effect of this diet on MeHg toxicity. MeHg suppressed the adaptive immune system and stimulated the innate immune system in rats in a diet-dependent fashion. The seal oil diet provided more resistance, while the fish oil diet rendered greater sensitivity to these effects of MeHg on the immune system. These results imply significant modulating effects of dietary fats on MeHg toxicity which may translate into more severe or protective clinical outcomes. Therefore, dietary fats are important factors to be considered in the risk assessment of MeHg exposure. Crown Copyright (c) 2006 Published by Elsevier Ireland Ltd. All rights reserved.