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May 1969

Effect of Catechol O-Methyl Transferase in Schizophrenia

Author Affiliations

Worcester, Great Britain; Soestdijk, Holland
From the Department of Psychiatry, Powick Hospital, Worcester, Great Britain (Drs. Hall and Hartridge), and Biochemisch Pharmaceutisch Laboratorium Enzympharm, Soestdijk, Holland (Mr. van Leeuwen).

Arch Gen Psychiatry. 1969;20(5):573-575. doi:10.1001/archpsyc.1969.01740170077011

THE WRITERS have attempted to treat a group of patients suffering from schizophrenia with catechol O-methyl transferase (OMT). It has been suggested that there may be a genetic deficiency of this enzyme in schizophrenia, either leading to inability to demethylate dietary dimethoxyphenylethylamine1 or causing disturbance in melanin metabolism with the production of abnormal hermine-like compounds,2 the resultant toxic substances causing the psychosis in each case.

Method  The enzyme preparation used was derived from etiolated peas; acute and chronic toxicity studies were carried out on rats, including tests for teratogenicity in three generations (by G.H.V.L.). The activity of the preparation was determined by paper chromatography, using 0.1 molar methionine as a methyl donor, and each cc contained 5 (±0.8) "units of activity" (1 "unit" = 1μ mol) of metanephrine formed in 30 minutes under standard conditions.3 No H3 epinephrine was available and a modified assay method was

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