Comparative studies on the metabolism of .BETA.-dimethylaminoethanol in the mouse brain and liver follosing administration of .BETA.-dimethyl-aminoethanol and its p-chlorophenoxyacetate, meclofenoxate.

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Abstract
1) After intravenous treatments of mice with equimolar doses of 14C-labeled β-dimethylaminoethanol (DMAE*) or its p-chlorophenoxyacetate [MF (DMAE*)], brain levels of DMAE* were found to be much higher in the latter treatment, due to the better penetration of the ester derivative, followed by hydrolysis. 2) DMAE* in the brain administered in either form of drugs was gradually phosphorylated to yield DMAE*-P, which was in turn converted to ptd-DMAE*, seemingly the end metabolite of DMAE* in the brain. 3) Acid-soluble and lipid cholines derived from DMAE* and MF (DMAE*) were also found in the brain. However, methylations of DMAE or its ester were attributed to occur in organs other than the brain, such as the liver, as revealed by relative incorporations of a labeled methyl group into lipid choline in the brain and liver after the treatment of methionine-methyl-14C.