Kontur P J, Fechter L D
Teratology. 1985 Aug;32(1):1-11. doi: 10.1002/tera.1420320102.
Manganese (Mn) can be neurotoxic when present in high concentrations. Neonatal animals show differential absorption, accumulation, and excretion of Mn relative to adults. If similar kinetic differences exist during gestation, then fetal animals may be susceptible to Mn neurotoxicity. The objective of this study was to examine maternal-fetal Mn transfer and the susceptibility of prenatal animals to Mn neurotoxicity. This was approached by studying the ability of Mn to cross the placenta and reach the fetal central nervous system using radiotracer and atomic absorption spectroscopy techniques. Manganese is thought to disrupt catecholamine neurotransmission in the central nervous system. This was examined in newborn rats by alpha-methyl-para-tyrosine induced catecholamine turnover and the development of the acoustic startle response. The results suggest that there are limits on fetal Mn accumulation under conditions of both normal and excessive dietary Mn levels. Manganese accumulation in the fetal brain after exposure to increased dietary Mn does not alter either dopamine or norepinephrine turnover or the development of the acoustic startle response. Excess Mn does not appear to be neurotoxic to fetal rats in spite of its limited accumulation in nervous tissue after gestational exposure.
锰（Mn）在高浓度时可能具有神经毒性。与成年动物相比，新生动物对锰的吸收、积累和排泄存在差异。如果在妊娠期存在类似的动力学差异，那么胎儿动物可能易受锰的神经毒性影响。本研究的目的是研究母体-胎儿间的锰转移以及产前动物对锰神经毒性的易感性。通过使用放射性示踪剂和原子吸收光谱技术研究锰穿过胎盘并到达胎儿中枢神经系统的能力来实现这一目标。锰被认为会扰乱中枢神经系统中的儿茶酚胺神经传递。通过α-甲基-对-酪氨酸诱导的儿茶酚胺周转以及听惊吓反应的发育，在新生大鼠中对此进行了研究。结果表明，在正常和过量饮食锰水平条件下，胎儿锰积累均存在限制。暴露于增加的饮食锰后，胎儿脑中的锰积累并未改变多巴胺或去甲肾上腺素的周转，也未改变听惊吓反应的发育。尽管妊娠暴露后锰在神经组织中的积累有限，但过量的锰似乎对胎儿大鼠没有神经毒性。
