Slotkin T A, Orband L, Cowdery T, Kavlock R J, Bartolome J
Toxicol Lett. 1987 Feb;35(2-3):285-95. doi: 10.1016/0378-4274(87)90218-9.
In order to assess the impact of prenatal exposure to methylmercury on sympathetic neurotransmission, effects on development of adrenergic receptor binding sites in peripheral tissues were evaluated. In the liver, methylmercury produced a dose-dependent increase in alpha 1-, alpha 2- and beta-receptor binding of radioligands throughout the first 5 weeks of postnatal life. Similarly, renal alpha-receptor subtypes showed increased binding capabilities, but binding to beta-receptor sites was reduced. At least some of the changes in receptors appear to be of functional significance, as physiological reactivity to adrenergic stimulation is altered in the same directions in these two tissues. The actions of methylmercury displayed tissue specificity in that the same receptor populations were largely unaffected in other tissues (lung, heart). These results suggest that methylmercury exposure in utero alters adrenergic responses through targeted effects on postsynaptic receptor populations in specific tissues.
为了评估产前接触甲基汞对交感神经传递的影响，研究人员对外周组织中肾上腺素能受体结合位点的发育影响进行了评估。在肝脏中，甲基汞在出生后的前5周内使放射性配体的α1、α2和β受体结合呈剂量依赖性增加。同样，肾脏α受体亚型的结合能力增强，但β受体位点的结合减少。受体的至少一些变化似乎具有功能意义，因为这两个组织中对肾上腺素能刺激的生理反应性朝着相同方向改变。甲基汞的作用表现出组织特异性，因为相同的受体群体在其他组织（肺、心脏）中基本未受影响。这些结果表明，子宫内接触甲基汞通过对特定组织中突触后受体群体的靶向作用改变肾上腺素能反应。
