Windebank A J
Exp Neurol. 1986 Oct;94(1):203-12. doi: 10.1016/0014-4886(86)90283-9.
Lead induces peripheral nerve segmental demyelination in rats. Arsenic and thallium produce a peripheral neuropathy characterized by axonal degeneration in humans. Mercury and thallium appear to damage both the peripheral and the central nervous system. It is not known whether this difference in effect is due to different molecular forms of the elements, to differential access to various compartments of the nervous system, or to intrinsically different properties of the elements. Using an in vitro model system of dorsal root ganglion neurons and morphometry of neurite outgrowth and myelination, we demonstrated that mercury and arsenic produce 50% inhibition of neurite outgrowth at 3.9 and 9.6 X 10(-6) M, respectively, whereas the same degree of inhibition is produced by 1.3 X 10(-4) M thallium and 3.3 X 10(-4) M lead. Lead also produces complete inhibition of myelination at 1 X 10(-6) M, suggesting that a primary effect on myelination is present in this model system as well as in the intact rodent.
铅会导致大鼠外周神经节段性脱髓鞘。砷和铊会引发一种以人类轴突变性为特征的外周神经病变。汞和铊似乎会损害外周神经系统和中枢神经系统。尚不清楚这种效应差异是由于元素的不同分子形式、进入神经系统不同区域的差异，还是由于元素本身不同的性质所致。利用背根神经节神经元的体外模型系统以及神经突生长和髓鞘形成的形态计量学方法，我们证明汞和砷分别在3.9×10⁻⁶ M和9.6×10⁻⁶ M时对神经突生长产生50%的抑制作用，而铊在1.3×10⁻⁴ M、铅在3.3×10⁻⁴ M时产生相同程度的抑制作用。铅在1×10⁻⁶ M时也会完全抑制髓鞘形成，这表明在该模型系统以及完整的啮齿动物中，对髓鞘形成均存在主要影响。
