G.M.J. Van Kempen

INTRACELLULAR LOCALIZATION OF GLUTAMATE DECARBOXYLASE, γ-AMINOBUTYRATE TRANSAMINASE AND SOME OTHER ENZYMES IN BRAIN TISSUE

IN studying the intracellular localization of glutamate decarboxylase (GAD, E.C. 4.1.1.15) in brain tissue of the rat, LDVTRUP (1961) and HILGERSOM (1962) could not detect any considerable amount of this enzyme in the mitochondrial fraction. SALGANICOFF and DE ROBERTIS (1963) prepared a mitochondrial fraction containing approximately 40 per cent of the GAD and 70-80 per cent of the y-aminobutyrate transaminase (GABAT, E.C. 2.6. I.-). By analysing this mitochondrial fraction on discontinous sucrose gradients, these authors showed the localization of both enzymes to be different. They suppose GABAT to be localized in mitochondria and GAD in nerve-endings. In view of the conflicting data on the intracellular localization of GAD we thought it desirable to reinvestigate this problem, including GABAT in the the analysis. The mitochondrial fraction was further studied by using centrifugation on continuous sucrose gradients, this technique being more refined than those used by DE ROBERTIS, PELLEGRINO DE IRALDI, RODRIGUEZ DE LORES ARNAIZ and SALGANICOFF (1 962) and WHITTAKER (1959). In all of the fractions cytochrome oxidase (E.C. 1.9.3.1), aspartate transaminase (GOT, E.C. 2.6.1. l), alanine transaminase (GPT, E.C. 2.6.1.2), lactate dehydrogenase (LDH, E.C. 1.1.1.27), alkaline phosphatase (E.C. 3.1.3.1), acid phosphatase (E.C. 3.1.3.2) and protein, were measured. and H. VELDSTRA*

Living with Huntington's disease: illness perceptions, coping mechanisms, and spouses' quality of life.

Chronic illness not only affects the life of those suffering from Huntington’s disease but also threatens the quality of life (QOL) of their spouses. In this study, we focus on Huntington’s disease (HD). The impact of HDonthe QOL of spouses has been hardly studied from a behavioral medicine or health psychology perspective. We hypothesize that spouses’ illness perceptions and coping mechanisms will contribute significantly to the prediction of their QOL. Illness perceptions, coping mechanisms, and the QOL of 90 spouses ofpatients with HD were assessed by meansof the Illness Perception Questionnaire, the COPE, and the Medical Outcome Study 36-item Short Form Health Survey, respectively. After controlling for demographic and illness-related variables, coping mechanisms explained a significant amount of variance of spouses’ role functioning. Given our results, more empirical and longitudinal research is justified on coping mechanisms and illness perceptions of spouses living with Huntington’s disease.

Does addition of low-dose flupentixol enhance the analgetic effects of low-dose amitriptyline in somatoform pain disorder?

&NA; In a double‐blind, crossover study, the effects of 75 mg amitriptyline alone during 5 weeks on pain intensity were compared with the effects of a combination of 75 mg amitriptyline and 3 mg flupentixol during 5 weeks in 34 patients with somatoform pain disorder. Both treatments resulted in a statistically significant reduction in pain. However, pain reduction in the combined treatment did not differ from that in the treatment with amitriptyline as a single drug. Neither tardive dyskinesias nor other serious side effects were observed. The results do not support the clinical practice of adding low‐dose neuroleptics to low‐dose antidepressants in the treatment of somatoform pain disorder.

Glutamate decarboxylase and γ-Aminobutyrate transaminase in developing rat brain

Le décarboxylase de glutamate (GAD) et le transaminase γ-aminobutyro-α-cétoglutarique (GABAT) ont été étudiés dans le cerveau du rat pendant le développement postnatal. Le résultat le plus frappant de cette recherche a été de montrer que le rapport de ces deux enzymes est à peu près constant au cours du développement. Ce rapport (GABAT/GAD) est de 2,5 à 3,7.

INTRACELLULAR LOCALIZATION OF PHENOL SULPHOTRANSFERASE IN RAT BRAIN

—The intracellular localization of phenol sulphotransferase in rat brain was studied The distribution pattern found after differential centrifugation closely resembles that of lactate dehydrogenase and does not change during postnatal development. The distribution of the enzyme in discontinuous and continuous sucrose gradients, however, shows a deviation from the lactate dehydrogenase pattern and a shift towards a higher sucrose concentration during development. In the adult the phenol sulphotransferase coincides with monoamine oxidase, succinate dehydrogenase and β‐glucuronidase. Disruption experiments, purification of mitochondria and electron microscopy exclude localization of phenol sulphotransferase in mitochondria. These studies support the idea of phenol sulphotransferase as a cytoplasmic enzyme with a preferential binding to or localization in oligodendroglial cells or, more probably, a specific type of synaptosomes.

Developmental patterns of sulphate activation and phenolsulphotransferase in rat brain.

Abstract— The formation of active suphate has been assayed in developing rat brain, the activity of the enzyme system being maximal at birth and thereafter decreasing gradually. The activity of phenolsuphotransferase, present in rat brain, is minimal at birth and increases gradually to the adult value.

Enzymatic sulfation of 4-methylumbelliferone

Die Aktivität von Sulfo-Transferasen wird mit Hilfe der 4-Methylumbelliferon-Methode nachgewiesen.

The Effects of Valproic Acid on Liver Function

To study a possible enzyme-inducing potency of valproic acid (VPA) in children, serum gamma-glutamyltranspeptidase (GGT) activity in serum and D-glucaric acid (GLA) excretion in urine were measured in 32 epileptic children who were on sodium valproate monotherapy (29.6 +/- 10.3 mg/kg/day). VPA did not affect GGT activity, but it selectively enhanced GLA excretion. To approach this phenomenon experimentally an attempt was made to induce a similar effect in animals. In guinea pigs it was possible to provoke a VPA induced rise in GLA excretion. In addition, vacuolisation of the cytoplasm of the hepatic parenchymal cells was observed. The question of the possible relationship between VPA hepatotoxicity and stimulation of GLA excretion remains to be answered.