title: A possible link between beta -carboline metabolism and infantile autism.
abstract: Benzodiazepine receptors and abnormal hepatic metabolism have been suggested to participate in several neuropsychiatric disorders including autism. Neuropsychoactive beta-carboline alkaloids as the potent ligands for benzodiazepine receptors are endogenously produced and exogenously supplied much more than benzodiazepines. 1-Methyl-1,2,3,4-tetrahydro-beta-carboline, a predominant alkaloid in humans and foodstuffs, is metabolically hydroxylated in liver. Although its in vivo levels show no difference between autistic and healthy children, the metabolic 6-hydroxylation is significantly decreased in autistic subjects. Therefore, it could be hypothesized that the reduced hepatic metabolism of 1-methyl-1,2,3, 4-tetrahydro-beta-carboline to 6-hydroxyl metabolite may be linked to the pathogenesis of infantile autism as suggested for autistic occurrence to involve the pathology similar to hepatic encephalopathy.
authors.affiliation: Department of Dental Pharmacology, Asahi University School of Dentistry, Hozumi, Gifu, Japan. hiro@dent.asahi-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Tsuchiya
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
mesh_terms: D001321:Autistic Disorder / Q000378:metabolism*; D002531:Cerebellum / Q000378:metabolism; D006246:Harmaline / Q000031:analogs & derivatives* / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D007223:Infant
chemical_list: C023426:tetrahydroharmane; D006246:Harmaline