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Hsu LL, Paul SM, Halaris AE, Freedman D X. 
“Rat Brain Aryl Acylamidase: Multiple Forms and Inhibition Effects of LSD. Serotonin and Related Compounds.”. 
Life Sci.. 1977;20(5):857-65.
The inhibition effects of LSD, serotonin (5HT) and related compounds on multiple forms of rat brain aryl acylamidase - (E.C.; AAA) were studied. Method, Adult male Sprague-Dawley rats (150-200 g) were decapitated. Their brains (without pineal glands) were homogenized in phosphate buffers then centrifuged, precipitated and dialyzed overnight. AAA enzyme activity was assayed by literature methods, and the effects on this of various compounds (all at 0.i mM) was evaluated. These included d- and l-LSD, 2-Br-LSD (BOL), T,N-dimethyl-tryptamine (DMT), 5-hydroxy-DMT (bufotenine) and d-amphetamine (all from the Center for Studies of Narcotic and Drug Abuse), 5HT. tryptamine, dopamine, norepinephrine, histamine, 5-methoxytryptamine and cyclic AMP (all from Sigma Chem.). mescaline (Aegis) and quipazine (MilesAmes). O-N;troacetanilide (ONAC; Eastman Kodak was used to determine the time course of AAA activity. Results Ammonium sulfate precipitation (33-60aturation) separated at least 2 forms of AAA. One fraction (AAA-1) showed a pH optimum at 7.5. the other (AAA-2) at 5.5. Significant (p 0.02) inhibition of AAA-1 at pH 7.5 was shown by d-LSD (68 0nhibition), BOL (55%). 5HT (26%) and tryptamine (15%). Other compounds inhibited AAA-1 8%. Only d-LSD and BOL showed significant and only moderate, inhibition of AAA-2 at pH 5.5. Inhibition by d-LSD and by BOL was 24% (p< 0.02). All others inhibited AAA-2 by 10%. Kinetic studies with AAA-1 indicated competitive inhibition by d-LSD with a Ki value of 4.90 + 0.61 mcM.
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