Matsumoto H, Chiba S, Kikuchi S, Wada T
Acta Neurol Scand. 1981 Dec;64(6):446-51. doi: 10.1111/j.1600-0404.1981.tb04422.x.
Experimental hepatoma of the rats was induced by chronic administration of 3'-methyl-dimethylamino-azobenzene. The folate level of the hepatoma-bearing rats tended to be low as compared with that of normal controls, and the co-existence of folate deficiency and reduced motor nerve conduction velocity of the dorsal nerve trunks appeared not uncommon. The hepatoma-bearing rats revealed the disturbance of serine to glycine conversion in serum, and folate administration to them prevented electrophysiological neuropathy along with normalization of serine to glycine conversion. Therefore, the reduced motor nerve conduction velocity could be at least in part the result of a metabolic impairment due to folate deficiency.
通过长期给予3'-甲基-二甲基氨基偶氮苯诱导大鼠实验性肝癌。与正常对照组相比，荷肝癌大鼠的叶酸水平往往较低，叶酸缺乏与背神经干运动神经传导速度降低并存的情况似乎并不少见。荷肝癌大鼠血清中丝氨酸向甘氨酸的转化出现紊乱，给予它们叶酸可防止电生理神经病变，同时丝氨酸向甘氨酸的转化恢复正常。因此，运动神经传导速度降低至少部分是叶酸缺乏导致代谢受损的结果。
