Kristensson K, Eriksson H, Lundh B, Plantin L O, Wachtmeister L, el Azazi M, Morath C, Heilbronn E
Acta Pharmacol Toxicol (Copenh). 1986 Nov;59(5):345-8. doi: 10.1111/j.1600-0773.1986.tb00182.x.
Sprague-Dawley rats were exposed to sublethal doses of manganese chloride during their postnatal development period up to 44 days of age. They showed transient clinical signs of disease and a decreased homovanillic acid (HVA) content in the striatum and hypothalamus between 15 and 22 days of age. The manganese content in the brain was increased 20-40 times during this period as determined with neutron activation analyses. In spite of this no structural damage or signs of maturation disturbances in the nervous system were found. Interruption of manganese exposure reversed the changes in HVA content.
在出生后发育至44日龄期间,将斯普拉格-道利大鼠暴露于亚致死剂量的氯化锰中。它们出现了短暂的疾病临床症状,并且在15至22日龄时纹状体和下丘脑中的高香草酸(HVA)含量降低。通过中子活化分析测定,在此期间大脑中的锰含量增加了20至40倍。尽管如此,未发现神经系统有结构损伤或成熟障碍的迹象。停止锰暴露可逆转HVA含量的变化。