The role of folate deficiency in electrophysiological neuropathy of experimental hepatoma of the rats

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Abstract
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.