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.
In experiments on 2-day-old rats (Wistar strain, our own breed), we studied the effect of altitude hypoxia (9000 m, 60 min) on the proportion of individual fatty acids in the brain (the cortex + the diencephalon + the cranial third of the mesencephalon). We found that hypoxia significantly altered the proportion of the various fatty acids, with a significant increase in the proportion of group n-3 polyenoic fatty acids at the expense of saturated and monoenoic acids. The results fully confirm the conception that one of the most important mechanisms responsible for the high resistance of new born mammals to oxygen deficiency is the ability of immature nervous tissue to activate, in particular, elongation (the elongation of fatty acids) and/or lipogenetic processes.
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).
In a group of 26 preterm newborn infants (gestational age 24-37 weeks, birth weight 560-2800 g) we followed the possible relationship between the birth weight and the proportion of polyunsaturated fatty acids n=3 in the blood serum. The blood samples were taken usually within 24 hours after birth, exceptionally within 48 hours. The newborns as well as their mothers did not receive antibiotics, tocolytics or hormonal therapy. We found a positive correlation between the birth weight and the proportion (expressed in %) of polyenoic fatty acids(n-3) in the blood serum. This relation could be expressed by the regression line (r=0.636, p<0.001, % FAn-3 = -1.166 + 0.00217 x birth weight in g. The value of Kruskal-Wallis criterion H was 15.158. The importance of such a relationship is discussed.
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.