Lack of Counteracting Effect of Liposomes on Benserazide-Induced Hyperprolactinemia

Abstract

Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduce serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seem to be capable to overcome the effects of the decarboxylase inhibition.

Benserazide‐induced gynaecomastia

“…Although benserazide's main pharmacological property is L‐aromatic amino acid decarboxylase activity, it is suggested that its structural similarity to levodopa may enable hypothalamic or pituitary dopamine‐receptor antagonist activity, hence blockage of tonic dopaminergic lactotroph suppression 3 …”