In children and adolescents (250 healthy subjects) serum dopamine-beta-hydroxylase (DBH) activity (23.95.2 to 57.117.5 μmol/min/ml) increases with the age between 3-10 years, later it decreases approximately by the age of 10-14 years. At the age of 21 to 60 years DBH level is stable. Our study described decreasing DBH activity in adolescents at the age of 10-14 years in the studied sample of healthy persons. Experimental animals (200 Wistar rats, 5-120 days old) show the same trend of enzymatic activity, similarly as in humans. DBH activity in rats is between 0.850.1 to 2.80.05 μmol/min/ml. This activity is highest in 5-day-old rats; it decreases till the age of 14 days and increases mainly in 14- to 35-day-old animals. Decrease of DBH activity in rats between 35 to 40 days is significant and corresponds to the reduction of DBH activity in adolescent humans (10-14 years). Adult rats (aged 90-120 days) show a stable DBH activity. DBH activity intermediately decreases in 10- to 14-year-old children. This decrease corresponds to the intermediate developmental changes of electrophysiological parameters (decreasing EEG activity in healthy adolescents occurs in 10-14 years old children). Puberty is coupled with intermediate decreasing of DBH activity in man and also in experimental animals in the period of prominent psychological and physiological changes.
The authors studied the effect of short-term (20 min) hypobaric hypoxia at simulated altitudes of 7000 and 9000 m on the peroxidation of lipids in the cerebral cortex, subcortical formations, medulla oblongata and cerebellum of the laboratory rat. In 5- and 21-day-old rats, increased lipoperoxidation was recorded in all the studied regions of the brain. Differences were observed in sensitivity to the degree of hypoxia. In 5-day-old rats the response to both exposures was the same, but in 21-day-old animals exposure at 7000 m stimulated peroxidation in the cerebral cortex only (at 9000 m in all the parts of the CNS examined). In 35-day-old and adult rats, changes in the malondialdehyde concentration were likewise found after exposure at 9000 m, but not in every compartment (in 35-day-old rats in the cerebral cortex and subcortical formations and in adult rats in the cerebral cortex). In young rats, 30 and 60 min after exposure to hypoxia the malondialdehyde concentration was still higher than in older animals.
The extent of ADP.Fe/NADPH-induced lipid peroxidation measured as production of thiobarbituric acid-reactive substances (TBARS) was determined in isolated membranes from cerebral cortex, heart and kidney of 21-days- old rats. The time course of lipid peroxidation showed higher production of TBARS in cerebral cortex than in heart and kidney. Our data indicate that high level of TBARS production is not due to high activity of NADPH oxidoreductase but due to high content of endogenous lipids in cerebral cortex membranes that could be modified. Higher production of TBARS in cerebral cortex is the result of higher content of lipids in cerebral cortex membranes because NADPH cytochrome c reductase activity in membranes of cerebral cortex is lower than that of heart and kidney.
Carnitine administration (by intraperitoneal injection) to 21-day-old-rats prevents the increase of thiobarbituric acid-reactive substances (index of lipid peroxidation and free radical damage) induced by 30 min hypobaric hypoxia in four different parts of the brain (cerebral cortex, subcortical structures, medulla oblongata and cerebellum).
The effect of normobaric oxygen atmosphere on hypoxia-enhanced lipid peroxidation in the brain cortex, subcortical structures, medulla oblongata and in the cerebellum was observed in 7- and 21-day-old and adult rats. The production of free oxygen radicals causing lipid peroxidation was assessed by the method described by Ohkawa et al. (1979). The rats were exposed for 30 min to 100 % oxygen atmosphere which significantly stimulated the production of malondialdehyde (MDA) in all the studied regions of the brain in 7- and 21-day-old male rats, and in the brain cortex and subcortical structures of adult males. Higher levels of MDA were found in the brain cortex of 7-day-old female rats only. Reoxygenation with pure oxygen after 30 min hypobaric hypoxia corresponding to 9000 m increased MDA production in all studied parts of the brain on both male and female rats 7- and 21-day-old. In adult rats significantly increased MDA production was only found in the brain cortex of male and female rats and in the subcortical structures of males. The exposition to hypobaric hypoxia followed by reoxygenation by atmospheric air enhanced MDA production in all studied regions of the brain in 7-day-old males and in the cerebellum of females; in 21-day-old rats of both sexes a significant increase of MDA was detected in all parts of the brain. In adult rats were found higher MDA levels in the cerebral cortex of both males and females.