Maternal diet during oogenesis is the major source of methylmercury in fish embryos
Maternal diet during oogenesis is the major source of methylmercury in fish embryos
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DOI：
10.1021/es0486263
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发表时间：
2005-05-15
影响因子：
11.4
通讯作者：
Sandheinrich, MB
中科院分区：
文献类型：
--
作者：
Hammerschmidt, CR;Sandheinrich, MB
甲基汞(MeHg)从母体转移到发育中的卵，可能会对鱼类早期生命阶段的发育产生不利影响。我们研究了母体将甲基汞转移到黑头鱼Pimephales proelas的卵子中，并评估了母体甲基汞负担与母体饮食在卵子发生期间对卵浓度的作用。幼鱼饲喂四种饲料中的一种直到性成熟(第一阶段)：对照饲料(0.06毫克汞g(-1)干重)和三种被甲基汞污染的饲料，分别为0.88(低)、4.11(中等)和8.46毫克(-1)(高)。在性成熟时，雌鱼与雄鱼配对，再次喂食四种饲料中的一种，并允许繁殖(第二阶段)。为了评估卵子发生过程中雌性饲料暴露对卵中甲基汞含量的影响，在第二阶段饲喂与第一阶段不同的饲料。在整个实验过程中，投喂相同饲料的鱼卵中甲基汞的平均浓度和负荷量随母鱼饲料中甲基汞含量的不同而不同，并与母鱼屠体中的水平呈正相关。然而，在不同的日粮处理中，鸡蛋中的甲基汞与身体中的甲基汞不成比例；饲喂对照组、低、中、高甲基汞日粮的成年人鸡蛋中的甲基汞平均为成人的14%、25%、32%和35%。对于幼鱼和达到性成熟后被甲基汞污染的饲料的鱼，卵中的甲基汞随着产卵前母亲饮食暴露的持续时间而迅速增加。此外，食用与幼鱼和性成熟鱼相同的污染饲料的鱼的卵中的甲基汞浓度与成鱼接触的时间没有关系，也没有明显高于仅在产卵前才喂食污染饲料的鱼的含量。这些结果表明，鱼卵中甲基汞的主要来源是母体成体在卵子发生过程中的饮食，而不是成体的身体负担。因此，胚胎野生鱼对甲基汞的暴露取决于成鱼在卵子发生期间猎物中的污染物水平，这可能会在一年内和年间发生变化。
Development of the early life stages of fishes can be affected adversely by methylmercury (MeHg) transferred from the maternal parent to the developing egg. We examined maternal transfer of MeHg to eggs of fathead minnows Pimephales promelas and evaluated the role of maternal MeHg burden versus that in the maternal diet during oogenesis on egg concentrations. Juvenile fish were fed one of four diets until sexual maturity (phase 1): A control diet (0.06 mu g of Hg g(-1) dry weight) and three that were contaminated with MeHg at 0.88 (low), 4.11 (medium), and 8.46 mu g of Hg g(-1) (high). At sexual maturity, female fish were paired with a male, again fed one of the four diets, and allowed to reproduce (phase 2). To assess the significance of female dietary exposure during oogenesis on MeHg in eggs, some fish were fed diets during phase 2 that differed from those during phase 1. Mean concentrations and burdens of MeHg in eggs from fish fed the same diet throughout the experiment varied with MeHg content of the maternal diet and were related positively to levels in the carcass of the maternal fish. However, MeHg in eggs was not proportional to that in carcasses among dietary treatments; MeHg in eggs from adults fed the control, low, medium, and high MeHg diets averaged 14%, 25%, 32%, and 35% of that in adults. For fish fed the control diet as juveniles and MeHg-contaminated diets after reaching sexual maturity, MeHg in eggs increased rapidly with duration of maternal dietary exposure prior to spawning. Moreover, concentrations of MeHg in eggs from fish fed the same contaminated diet as both juveniles and sexually mature adults were not related to the duration of adult exposure, and they were not appreciably greater than those from fish fed contaminated diets only just prior to spawning. These results indicate that the diet of the maternal adult during oogenesis, and not adult body burden, is the principal source of MeHg in fish eggs. Accordingly, the exposure of embryonic wild fishes to MeHg depends on levels of the contaminant in prey of the adult during oogenesis, which can vary intra- and interannually.