Nicotinic acid or N-methyl nicotinamide prolongs elevated brain dopa and dopamine in L-dopa treatment

A peripheral dopa decarboxylase inhibitor, benserazide, was given ip, followed by intubation with L-dopa. Brain dopa and DA levels were elevated maximally between 0.5-2.5 hr and 1.0-2.5 hr, respectively. Dopa in serum, liver, and brain were at control values after 4 hr. Supplementation of dopa with NAM or NAC, as possible methyl group acceptors to lower catabolism of DA, showed that NAM had no effect on DA levels or on SAM. However, with both NAC and N-methyl NAM (a methylated compound intended as a control) at time periods where dopa and DA were normally decreasing, the brain levels were increased over control values with benserazide and dopa alone. NAC or N-methyl NAM appeared to extend the period of elevated brain DA levels with L-dopa treatment. The mechanism responsible for these results is uncertain.