[Tryptophan metabolism and oligophrenia (author's transl)].

After dealing with the biochemistry of tryptophan metabolism the most important results obtained in humans are presented. Special emphasis is given to the hereditary defects of tryptophan metabolism associated with mental retardation and convulsions due to lack of pyridoxine. The author's findings demonstrate the existence of a hereditary disturbance of the tryptophan metabolism via kynurenine in a certain part of oligophrenic patients.

[Tryptophan metabolism research in oligophrenic children. 4.: Activity and possibility of activating hepatic kynureninase after vitamin B6 treatment].

In 8 selected test persons of the 3rd series of experiments who were showing signs of pathological kynureninase activity, hepatic kynureninase was again established after 3 week's treatment with large doses of vitamin B6. The enormous in-vivo activation of the kynureninasis established goes to prove that apoenzyme synthesis may be stimulated by pyridoxine. On the basis of these results and the relative frequency of disorders dependent on B6, the question arises whether children from endangered families should not be given prophylactic vitamin B6 treatment from birth.

[Determination of kynureninase activity in oligophrenic children with hereditary taint, before and after vitamin B6 treatment].

Kynureninase activity assay in oligophrenic children with hereditary taint, before and after treatment with vitamin B6. The hepatic kynureninase activity was assayed in 25 oligophrenic children with hereditary taint, and having a positive tryptophan load test. Eight cases (32%) showed an enzyme activity below the 2-s limit; in two cases, the pathologic enzyme activity could be almost normalized by addition of higher P-5-P concentrations.