Phospholipids composition of cell nuclei of rat’s brain in dynamics of normal ontogenesis and after hypoxia (original) (raw)
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Hypoxia-Induced Lipid Peroxidation in the Brain During Postnatal Ontogenesis
Physiological Research, 2012
Reactive oxygen species (ROS) are common products of the physiological metabolic reactions, which are associated with cell signaling and with the pathogenesis of various nervous disorders. The brain tissue has the high rate of oxidative metabolic activity, high concentration of polyunsaturated fatty acids in membrane lipids, presence of iron ions and low capacity of antioxidant enzymes, which makes the brain very susceptible to ROS action and lipid peroxidation formation. Membranes of brain cortex show a higher production of thiobarbituric acid-reactive substances (TBARS) in prooxidant system (ADP.Fe3+/NADPH) than membranes from the heart or kidney. Lipid peroxidation influences numerous cellular functions through membrane-bound receptors or enzymes. The rate of brain cortex Na+,K+-ATPase inhibition correlates well with the increase of TBARS or conjugated dienes and with changes of membrane fluidity. The experimental model of short-term hypoxia (simulating an altitude of 9000 m for ...
Neuroscience Research, 2003
Hypoxia Á/ischemia is a common cause of neonatal brain damage producing serious impact on cerebral maturation. This report demonstrates that rats submitted to hypoxia Á/ischemia present a marked decrease in hippocampal gangliosides, phospholipids and cholesterol contents as from 7 days after the injury. Although chromatographic profiles of the different ganglioside species (GM1, GD1a, GD1b, and GT1b) from the hippocampus of hypoxic-ischemic hippocampi groups (HI) were apparently unaffected, as compared with controls, there were quantitative absolute reductions in HI. The phospholipid patterns were altered in HI as from the 14th to the 30th day after the injury, where phosphatidylcholine (PC) quantities were higher than phosphatidylethanolamine (PE); additionally, the cardiolipin band was detected only in hippocampi of control adult rats. In general, the absolute quantities of phospholipids were lower in HI than in correspondent controls since 7th day after the injury. Considering that reported effects were maintained, we suggest they express a late biochemical response triggered by the neonatal hypoxic-ischemic episode; the consequences would be cell death and a delay on brain development, expressed by a reduction on synaptogenesis and myelinogenesis processes.
Scientific Reports, 2018
Neonatal hypoxic-ischaemic (HI) encephalopathy is among the most serious complications in neonatology. In the present study, we studied the immediate (0 hour), subacute (36 hours) and late (144 hours) responses of the neonatal brain to experimental HI insult in laboratory rats. At the striatal level, the mass spectrometry imaging revealed an aberrant plasma membrane distribution of Na + /K + ions in the oedema-affected areas. The failure of the Na + /K + gradients was also apparent in the magnetic resonance imaging measurements, demonstrating intracellular water accumulation during the acute phase of the HI insult. During the subacute phase, compared with the control brains, an incipient accumulation of an array of N-acylphosphatidylethanolamine (NAPE) molecules was detected in the HI-affected brains, and both the cytotoxic and vasogenic types of oedema were detected. In the severely affected brain areas, abnormal distributions of the monosialogangliosides GM2 and GM3 were observed in two-thirds of the animals exposed to the insult. During the late stage, a partial restoration of the brain tissue was observed in most rats in both the in vivo and ex vivo studies. These specific molecular changes may be further utilized in neonatology practice in proposing and testing novel therapeutic strategies for the treatment of neonatal HI encephalopathy.
International Journal of Molecular Sciences, 2022
Hypoxia is damaging to the fetus, but the developmental impact may vary, with underlying molecular mechanisms unclear. We demonstrate the dependence of physiological and biochemical effects of acute prenatal hypoxia (APH) on sex and gestational age. Compared to control rats, APH on the 10th day of pregnancy (APH-10) increases locomotion in both the male and female offspring, additionally increasing exploratory activity and decreasing anxiety in the males. Compared to APH-10, APH on the 20th day of pregnancy (APH-20) induces less behavioral perturbations. ECG is changed similarly in all offspring only by APH-10. Sexual dimorphism in the APH outcome on behavior is also observed in the brain acetylation system and 2-oxoglutarate dehydrogenase reaction, essential for neurotransmitter metabolism. In view of the perturbed behavior, more biochemical parameters in the brains are assessed after APH-20. Of the six enzymes, APH-20 significantly decreases the malic enzyme activity in both sexes...
Lipid peroxidation in developing fetal guinea pig brain during normoxia and hypoxia
Developmental Brain Research, 1989
Lipid peroxidation in the fetal guinea pig brain was studied at 40, 50, and 60 days of gestation. Conjugated dienes and fluorescent compounds, indices of lipid peroxidation, peaked at 35 days of gestation, decreased by 45 days, and remained at that level until birth. The higher levels of peroxidation products in early gestational periods (30-40 days) suggest that either the anti-oxidant mechanisms for scavenging oxygen free-radicals and further metabolizing oxidation products are underdeveloped, or the rate of peroxidation is higher than periods near term. Prenatal hypoxia increased the levels of conjugated dienes and fluorescent products in the brains of preterm (50 days) and term (60 days) fetuses. Brain homogenates incubated in air at 37 °C underwent rapid lipid peroxidation as measured by the level of thiobarbituric acid (TBA)-reactive substances. However, term brain showed a higher rate of peroxidation and attained higher steady state levels of TBA-reactive substances than preterm brain. This may be due to the higher levels and degrees of unsaturation in fatty acids in term brain. Following hypoxia, term brain showed 5 times the rate of lipid peroxidation and a 3fold increase in total TBA-reactive substances over controls. These studies show that a significant degree of lipid peroxidation is occurring in the fetal brain during gestation and that the developing brain is more susceptible to lipid peroxidation near term. Furthermore, prenatal hypoxic stress further increases the susceptibility of the brain to peroxidative reactions.
In vivo effect of chronic hypoxia on the neurochemical profile of the developing rat hippocampus
Developmental Brain Research, 2005
The cognitive deficits observed in children with cyanotic congenital heart disease suggest involvement of the developing hippocampus. Chronic postnatal hypoxia present during infancy in these children may play a role in these impairments. To understand the biochemical mechanisms of hippocampal injury in chronic hypoxia, a neurochemical profile consisting of 15 metabolite concentrations and 2 metabolite ratios in the hippocampus was evaluated in a rat model of chronic postnatal hypoxia using in vivo 1 H NMR spectroscopy at 9.4 T. Chronic hypoxia was induced by continuously exposing rats (n = 23) to 10% O 2 from postnatal day (P) 3 to P28. Fifteen metabolites were quantified from a volume of 9-11 Al centered on the left hippocampus on P14, P21, and P28 and were compared with normoxic controls (n = 14). The developmental trajectory of neurochemicals in chronic hypoxia was similar to that seen in normoxia. However, chronic hypoxia had an effect on the concentrations of the following neurochemicals: aspartate, creatine, phosphocreatine, GABA, glutamate, glutamine, glutathione, myoinositol, N-acetylaspartate (NAA), phosphorylethanolamine, and phosphocreatine/creatine (PCr/Cr) and glutamate/glutamine (Glu/Gln) ratios ( P b 0.001 each, except glutamate, P = 0.04). The increased PCr/Cr ratio is consistent with decreased brain energy consumption. Given the well-established link between excitatory neurotransmission and brain energy metabolism, we postulate that elevated glutamate, Glu/Gln ratio, and GABA indicate suppressed excitatory neurotransmission in an energy-limited environment. Decreased NAA and phosphorylethanolamine suggest reduced neuronal integrity and phospholipid metabolism. The altered hippocampal neurochemistry during its development may underlie some of the cognitive deficits present in human infants at risk of chronic hypoxia. D 2005 Elsevier B.V. All rights reserved.
Brain Research, 1993
The effect of hypoxia on the structure and function of the synaptosomal membranes and myelin fraction (glial cells, neuronal cell bodies and axonal membranes) was investigated by measuring Na~,K+-ATPase activity and levels of lipid peroxidation products in cerebral cortical synaptosomal membranes and myelin fractions obtained from newborn piglets. Hypoxic hypoxia was induced and cerebral hypoxia was documented as a decrease in the ratio of phosphocreatine to inorganic phosphate (PCr/Pi) using 31P_NMR spectroscopy. PCrfPi decreased from baseline of 2.93 + 0.76 to 0.61 + 0.36 during hypoxia. The synaptosomal membrane Na +,K+-ATPase activity decreased from a control value of 56.6 _-+_ 3.7 to 40.4 + 6.0 p.mol Pi/mg protein/h during hypoxia. The level of conjugated dienes increased from zero (reference value) to 4.5 _+ 2.7 nmol/mg lipid and the level of fluorescent compounds increased from 23.5_ 2.2 to 92.6_+ 46.4 ng quinine sulfate/mg lipid in the synaptosomal membranes during hypoxia. No change in myelin fraction Na+,K+-ATPase activity or levels of lipid peroxidation products were noted. These data indicate that synaptosomal membranes, rich in polyunsaturated fatty acids, are more susceptible to oxygen free radical mediated lipid peroxidative damage during hypoxia.
Anti-oxidant enzymes in fetal guinea pig brain during development and the effect of maternal hypoxia
Developmental Brain Research, 1988
The development of the anti-oxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase was studied in the fetal guinea pig brain at 40, 45, 50, 55, and 60 days of gestation. The activities of these enzymes remained constant during 30-45 days of gestation and increased significantly during the 45-60 day period, with the exception of superoxide dismutase, which remained unchanged throughout the gestational period. The enzyme activities in fetal brain tissue at every gestational age were unaffected by maternal hypoxia (inspired oxygen, 7% for 40 min). The concurrent development of glucose-6-phosphate dehydrogenase, glutathione reductase, and glutathione peroxidase during 45-60 days of gestation indicates an increased ability of the fetal brain to detoxify lipid peroxidation products by reinforcing the glutathione system. The results of this study indicate that the anti-oxidant enzymatic defense mechanisms in the guinea pig brain are fairly mature at birth. However, these mechanisms are underdeveloped during the early stages of gestation and, therefore, during this period the brain might be at potential risk for lipid peroxidative damage under conditions leading to increased formation of oxygen free radicals. were purchased from Sigma. Pregnant, Dunkin Hartley guinea pigs of 30, 35, 40, 45, 50, 55, and 60 days of Correspondence: O.P. Mishra, Department of Physiology, Room A201, Richards Bldg., G/4,