Dopamine beta hydroxylase (DBH) plasma activity in childhood mental disorders.

BACKGROUND: Developmental study of dopaminergic and noradrenergic systems in child psychiatric disorders are rare. DBH activity is one of noradrenergic biochemical marker that is correlate in psychiatry to clinical and genetic data. OBJECTIVES: The main aim of the present study was to measure DBH activity at the onset of acute schizophrenia and depressive disorder in children and adolescents without pharmacological treatment and to compare these values with DBH activity in healthy controls. The authors also investigated untreated ADHD children. METHODS: We examined 42 control healthy children, 15 children non-treated with acute schizophrenia, 15 non-treated children with acute depressive disorders and 30 non-treated ADHD children, all in age 7-14. Plasma DBH level was provided by Nagatsu (1972; 1974). Depressed children were reexamined after clinical remission. RESULTS: DBH activity is statistically significantly decreased in non-treated depressive disorder and ADHD in children and adolescents. DBH activity is normalised during antidepressant therapy in child depression. Child schizophrenia patients present with normal DBH activity. CONCLUSION: These results are similar to the results that have been observed in adult patients with schizophrenia and depression and in previous studies of DBH activity in children with ADHD. These results also indicate hypoactivity of the noradrenergic system in children with ADHD and depression.

Activity of lactate dehydrogenase in serum and cerebral cortex of immature and mature rats after hypobaric hypoxia.

In our previous studies we have found both an increase of lipid peroxidation damage (expressed as levels of thiobarbituric acid-reactive substances) in brain and plasma lactate concentration in 21-day-old rats after a 30-min exposure to hypobaric hypoxia. Pretreatment of rats with L-carnitine decreased both parameters. The aim of our present study was to determine if the L-carnitine-dependent decrease of plasma lactate could be due to a modification of lactate dehydrogenase (LDH) activity. We followed brain and blood serum LDH activity of 14-, 21- and 90-day-old Wistar rats. We found an increase of brain LDH activity with age. However, we did not observe any significant differences in LDH activity after exposure to hypobaric hypoxia or L-carnitine pretreatment. In contrast to brain, serum LDH activity did not show any clear age-dependence. The hypoxia exposure increased LDH activity of 21-day-old rats only. Pretreatment of rats with L-carnitine decreased serum LDH activity of 21- and 90-day-old rats probably due to membrane stabilizing role of L-carnitine. In conclusions, acute hypobaric hypoxia and/or L-carnitine pretreatment modified serum but not brain LDH activity.

Hypoxia-induced lipid peroxidation in rat brain and protective effect of carnitine and phosphocreatine.

The exposure to hypobaric hypoxia increased lipid peroxidation as indicated by thiobarbituric acid-reactive substances [TBARS] in rat brain. Plasma lactate/pyruvate ratio was used as a marker of hypoxia. We compared the protective effect of alpha-tocopherol with the effect of L-carnitine or phosphocreatine. Rats pretreated with alpha-tocopherol, L-carnitine, or phosphocreatine had lower TBARS levels after the exposure to hypobaric hypoxia. However, lactate/ pyruvate ratio was improved only in rats pretreated with L-carnitine or phosphocreatine. We conclude from our data that, contrary to alpha-tocopherol, protective effects of L-carnitine and phosphocreatine administrations are due to their regulation of metabolic reactions during hypobaric hypoxia rather than to their scavenger activity.