Changes in lipid metabolism in traumatized spinal cord.
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Adenosine Triphosphatases↗
Biomedical subjects
P Demediuk
Publications and source records attributed to P Demediuk.
Spinal cord injury and protection.
Subsequent to traumatic injury of the spinal cord, a series of pathophysiological events occurs in the injured tissue that leads to tissue destruction and paraplegia. These include hemorrhagic necrosis, ischemia, edema, inflammation, neuronophagia, loss of Ca2+ from the extracellular space, and loss of K+ from the intracellular space. In addition, there is trauma-initiated lipid peroxidation and hydrolysis in cellular membranes. Both lipid peroxidation and hydrolysis can damage cells directly; hydrolysis also results in the formation of the biologically active prostaglandins and leukotrienes (eicosanoids). The time course of membrane lipid alterations seen in studies of antioxidant interventions suggests that posttraumatic ischemia, edema, inflammation, and ionic fluxes are the result of extensive membrane peroxidative reactions and lipolysis that produce vasoactive and chemotactic eicosanoids. A diverse group of compounds has been shown to be effective in ameliorating spinal cord injury in experimental animals. These include the synthetic glucocorticoid methylprednisolone sodium succinate (MPSS); the antioxidants vitamin E, selenium, and dimethyl sulfoxide (DMSO); the opiate antagonist naloxone; and thyrotropin-releasing hormone (TRH). With the exception of TRH, all of these agents have demonstrable antioxidant and/or anti-lipid-hydrolysis properties. Thus the effectiveness of these substances may lie in their ability to quench membrane peroxidative reactions or to inhibit the release of fatty acids from membrane phospholipids, or both. Whatever the mode of action, early administration appears to be a requirement for maximum effectiveness.
Animals↗
Membrane lipid changes in laminectomized and traumatized cat spinal cord.
Free fatty acid (FFA), diacylglycerol (acyl2Gro), icosanoid, phospholipid, and cholesterol levels were measured in samples of cat spinal cord (L2) that were frozen in situ with vertebrae intact, at various times after laminectomy, and at various times after laminectomy with compression trauma to the spinal cord. Tissue samples either were grossly dissected into gray and white portions prior to FFA and acyl2Gro analysis or were used whole for the other lipid types. Gray matter total FFA and acyl2Gro values were abnormally high in samples frozen with vertebrae intact and in those frozen 10 min after laminectomy. This indicates that the surgical procedures resulted in some perturbation of spinal cord lipid metabolism. If the experimental animals were allowed to recover for 90 min after laminectomy, the gray matter FFA and acyl2Gro levels were greatly reduced. Compression of the spinal cord with a 170-g weight for 1, 3, or 5 min (following 90 min of recovery after laminectomy) caused significant elevations of total FFA, acyl2Gro, icosanoids, and phosphatidic acid and significant decreases in ethanolamine plasmalogens and cholesterol. Among the total FFA, arachidonic acid was found to have the largest relative increase. Comparisons of gray and white matter demonstrate that, in general, changes in white matter FFA and acyl2Gro were similar to those seen in gray matter. However, the increases in white matter levels of FFA and acyl2Gro were delayed, occurring after the elevations in gray matter. For some FFA (e.g., arachidonate), the rise in white matter occurred as gray matter levels were decreasing. This suggests that the initial alteration in spinal cord lipid metabolism after trauma was in gray matter but, with time, spread radially into white matter.
Animals↗
The degradation of phospholipids, formation of metabolites of arachidonic acid, and demyelination following experimental spinal cord injury.
Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.
Animals↗
Lipid hydrolysis and peroxidation in injured spinal cord: partial protection with methylprednisolone or vitamin E and selenium.
Compression trauma of the cat spinal cord induces a very rapid alteration in the lipid metabolism of cellular membranes, including lipid hydrolysis with release of fatty acids including arachidonate, production of biologically active eicosanoids, and loss of cholesterol. This disturbance of cellular membranes can directly damage cells and can lead to the secondary development of tissue ionic imbalance, ischemia, edema, and inflammation with neuronophagia. Pretreatment with either the synthetic glucocorticoid methylprednisolone sodium succinate (MPSS) or the antioxidants vitamin E and selenium (Se) completely prevented the loss of cholesterol and partially inhibited lipolysis and prostanoid production. Treatment with MPSS significantly reduced the postinjury tissue necrosis and paralysis. Preliminary evidence indicates that pretreatment with vitamin E and Se also protected against the effects of spinal cord injury (SCI). We speculate that the ability of these agents to preserve function after SCI may, in part, reside in their capacity to limit the trauma-induced changes in lipid metabolism.
Animals↗
Neurobehavioral effects of chronic choline-containing diets on the adult and aging C57BL/6NNIA mouse brain.
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Aging↗
Effects of plasmenylethanolamine on the dynamic properties of the hydrocarbon region of mixed phosphatidylcholine-phosphatidylethanolamine aqueous dispersions. A spin label study.
Spin-labeled aqueous dispersions of total phospholipid extracts from whole brains of hibernating hamsters and rats chronically consuming ethanol were compared with dispersions from control animals. Order parameter values and approximate rotational correlation times for the nitroxide spin labels indicated that ethanol consumption results in an adaptive decrease in bilayer membrane fluidity, while hibernation produces increases in fluidity. Since it has been proposed that changes in plasmenylethanolamine such as those seen with hibernation play a role in the homeoviscous adaptation of brain membranes, electron spin resonance studies using aqueous phospholipid dispersions containing equimolar mixtures of rat brain phosphatidylethanolamine and phosphatidylcholine, or synthetic dioleylphosphatidylcholine and dioleylphosphatidylethanolamine, and brain plasmenylethanolamine were performed. The molar amount of plasmenylethanolamine was varied within the ethanolamineglycerophospholipid fraction of each dispersion. Order parameter values of spin labels in liposomes containing brain phosphatidylcholine and phosphatidylethanolamine increased in parallel with increases in plasmenylethanolamine concentrations, indicating that fluidity was decreasing. Liposomes composed of synthetic dioleyl phospholipids exhibited biphasic changes in order parameter (S) values as plasmenylethanolamine replaced the diacyl form. Below 30% (mol%) plasmenylethanolamine, S values decreased, while above 30%, S values were seen to increase; indicating an initial fluidization, followed by a decrease in fluidity.
Animals↗
Synaptosomal and brain mitochondrial lipids in hibernating and cold-acclimated golden hamsters.
Synaptosomes and mitochondria were isolated from the brains of warm-adapted, hibernating, and cold-acclimated golden hamsters (Mesocricetus auratus). Lipid extracts of these subcellular fractions were prepared and assayed for plasmenylethanolamine (ethanolamine plasmalogen) and cholesterol levels. The ganglioside composition of synaptosomes was also determined. Samples from the hibernating animals showed characteristic changes in lipid composition. These changes include decreases in plasmenylethanolamine levels and a shift in the ganglioside composition toward a higher percentage of the more polar gangliosides. Those animals which were exposed to cold and did not hibernate (cold-acclimated) showed no such changes. Fatty acid analyses of synaptosomal and mitochondrial ethanolamine glycerophospholipids demonstrated a similar trend. Samples from hibernators showed decreases in 16:0, 18:0, and 22:6 (n-3), and increases in 16:1, 18:1, and 20:4 (n-6) fatty acids. No changes were detectable in samples from cold-acclimated animals, indicating that hibernating and cold-acclimated hamsters represent chemically distinct populations.
Acclimatization↗
Effects of chronic consumption of ethanol and low-thiamin, low-protein diets on the lipid composition of rat whole brain and brain membranes.
Four groups of rats were used in a nutritionally-controlled study of effects of chronic ethanol consumption on brain membrane lipid composition. Rats chronically consuming ethanol were fed high-nutrient or low-thiamin, low-protein diets. After 4 months, lipid analyses were performed on brains, brain microsomes and myelin from each group and from pair-fed, non-ethanol controls. Among the effects of ethanol was an increase of the relative proportion of cholesterol in microsomal lipids while there was decrease of it in myelin. Ethanol also increased plasmenylethanolamine while decreasing phosphatidylethanolamine proportions in myelin and in whole brain lipids, decreased the total lipid phosphorus of whole brain, and elevated the proportion of phosphatidylserine in microsomal and whole brain lipids. Effects of poor diet generally did not interfere with ethanol effects except in the case of microsomal lipids, where it apparently prevented an ethanol-induced increase in proportion of cholesterol. These changes may be adaptive responses to the fluidizing effect of ethanol on membranes.
Animals↗