Molecular and Environment Sciences Group, Department of Geological Sciences, University of Saskatchewan, 114 Science Place, Saskatoon, Saskatchewan S7N 5E2, Canada.
Metallomics. 2019 Mar 20;11(3):621-631. doi: 10.1039/c8mt00315g.
Mercury is one of the most toxic elements threatening the biosphere, with levels steadily rising due to both natural and human activities. Selenium is an essential micronutrient, required for normal development and functioning of many organisms. While selenium is known to counteract mercury's toxicity under some conditions, to date information about the mercury-selenium relationship is fragmented and often controversial. As part of a systematic study of mercury and selenium interactions, zebrafish (Danio rerio) larvae (a model verterbrate) were exposed to methylmercury chloride or mercuric chloride. The influence of pre- and post-treatment of selenomethionine on the level and distribution of mercury and selenium in the brain and eye sections, as well as on toxicity, were examined. Selenomethionine treatment decreased the amount of maternally transfered mercury in the larval brain. Selenomethionine treatment prior to exposure to mercuric chloride increased both mercury and selenium levels in the brain but decreased their toxic effects. Conversely, methylmercury levels were not changed as a result of selenium pre-treatment, while toxicity was increased. Strikingly, both forms of mercury severely disrupted selenium metabolism, not only by depleting selenium levels due to formation of Hg-Se complexes, but also by blocking selenium transport into and out of tissues, suggesting that restoring normal selenium levels by treating the organism with selenium after mercury exposure may not be possible. Disruption of selenium metabolism by mercury may lead to disruption in function of selenoproteins. Indeed, the production of thyroid hormones by selenoprotein deiodinases was found to be severely impaired as a result of mercury exposure, with selenomethionine not always being a suitable source of selenium to restore thyroid hormone levels.
汞是威胁生物圈的最有毒元素之一，由于自然和人类活动，其水平一直在稳步上升。硒是一种必需的微量元素，是许多生物体正常发育和功能所必需的。虽然已知在某些条件下硒可以拮抗汞的毒性，但迄今为止，关于汞-硒关系的信息是零散的，而且常常存在争议。作为对汞和硒相互作用的系统研究的一部分，斑马鱼（Danio rerio）幼虫（一种模式脊椎动物）暴露于甲基汞氯化物或氯化汞中。研究了硒代蛋氨酸预处理和后处理对大脑和眼部切片中汞和硒水平以及毒性的影响。硒代蛋氨酸处理减少了母体转移到幼虫大脑中的汞量。在暴露于氯化汞之前进行硒代蛋氨酸处理会增加大脑中的汞和硒水平，但会降低其毒性作用。相反，由于形成 Hg-Se 复合物，硒预处理不会改变甲基汞的水平，但会增加其毒性。引人注目的是，两种形式的汞都严重破坏了硒的新陈代谢，不仅由于形成 Hg-Se 复合物导致硒水平下降，而且由于阻止硒进出组织的运输，这表明在暴露于汞后通过用硒处理生物体来恢复正常的硒水平可能是不可能的。汞对硒代谢的破坏可能导致硒蛋白的功能障碍。事实上，发现甲状腺激素的产生受到严重损害，这是由于脱碘酶的硒蛋白被汞暴露所致，而硒代蛋氨酸并不总是恢复甲状腺激素水平的合适硒源。
