Lipid Hydroperoxides Inhibit Reacylation of Phospholipids in Neuronal Membranes

Zaleska, Małgorzata; Wilson, David F.

doi:10.1111/j.1471-4159.1989.tb10925.x

Cited by 61 publications

(16 citation statements)

References 37 publications

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“…In agreement with published data, we too found increased endogenous TBARSs in older RBCs, suggesting a higher level of lipid peroxidation in aged erythrocytes. 25,34 Hydroperoxides have been shown to exert an inhibitory effect on the PL reacylating reactions 35 and could contribute to the impairment of fatty acid esterification found in aged erythrocytes 26,36 as well as to the loss of PUFAs and PLs observed with RBC aging in the present and previous works. However, endogenous TBARS levels were higher in IRBCs and also in young and medium URBCs compared with NRBCs of the same densities.…”

Section: Discussionsupporting

confidence: 58%

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Omodeo‐Salè

Motti

Basilico

et al. 2003

Blood

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Red blood cells infected with Plasmodium falciparum (IRBCs) undergo changes primarily in their membrane composition that contribute to malaria pathogenesis. However, all manifestations (eg, anemia) cannot be accounted for by IRBCs alone. Uninfected erythrocytes (URBCs) may play a role, but they have been underresearched. We wanted to document changes in the erythrocyte membrane that could contribute to URBC reduced life span and malaria-associated anemia. Human erythrocytes were cultured with P falciparum and washed at the trophozoite stage. IRBCs and URBCs were separated on Percoll density gradient, thus obtaining erythrocyte fractions of different densities/ages. IRBC-and URBCpurified membranes were analyzed and compared with control normal erythrocytes (NRBCs) of the same age, from the same donor, kept in the same conditions. P falciparum accelerated aging of both IRBCs and URBCs, causing a significant shift in the cell population toward the denser (old) fraction. Protein, phospholipid, and cholesterol content were reduced in IRBCs and young URBCs. Young and medium uninfected fractions had higher levels of lipid peroxidation and phospholipid saturation (because of the loss of polyunsaturated fatty acids, PUFAs) and lower phosphatidylserine. In IRBCs, thiobarbituric reactive substances (TBARSs) were higher, and PUFAs and phosphatidylserine lower than in NRBCs and URBCs. In comparison, trophozoite membranes had lower phospholipid (particularly sphingomyelin and phosphatidylserine) and cholesterol content and a higher degree of saturation. Parasiteinduced peroxidative damage might account for these modifications. In summary, we demonstrated that membrane damage leading to accelerated senescence of both infected and uninfected erythrocytes will likely contribute to malaria anemia. (Blood. 2003;102:705-711)

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Section: Discussionsupporting

confidence: 58%

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Omodeo‐Salè

Motti

Basilico

et al. 2003

Blood

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“…The lipid hydroperoxides are known to inhibit reacylation of phospholipids in neuronal membranes (68). This inhibition may constitute another mechanism whereby oxidative processes contribute to necrotic cell death in neural cells (24).…”

Section: Involvement Of Multiple Forms Of Pla 2 In Necrosismentioning

confidence: 99%

Biochemical Aspects of Neurodegeneration in Human Brain: Involvement of Neural Membrane Phospholipids and Phospholipases A2

2004

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Neural membrane phospholipids are hydrolyzed by a group of enzymes known as phospholipases. This process results in the generation of second messengers such as arachidonic acid, eicosanoids, platelet activating factor, and diacylglycerols. High levels of these metabolites are neurotoxic and are associated with neurodegeneration. The collective evidence from many studies suggests that neural membrane phospholipid metabolism is disturbed in neural trauma and neurodegenerative diseases. This disturbance is caused by the stimulation of phospholipases A2. Stimulation of these enzymes produces changes in membrane permeability, fluidity, and alteration in ion homeostasis. Low calcium influx produces mild oxidative stress and results in neurodegeneration promoted by apoptosis, whereas a calcium overload generates high oxidative stress and causes neurodegeneration associated with necrosis. Alterations in phospholipid metabolism along with the accumulation of lipid peroxides and compromised energy metabolism may be responsible for neurodegeneration in ischemia, spinal cord trauma, head injury, and Alzheimer disease. The synthesis of phospholipases A2 inhibitors that cross the blood-brain barrier without harm may be useful for the treatment of acute neural trauma and neurodegenerative diseases.

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“…However, in a previous study of cerebral metabolism during ischemic hypoxia induced by hyperventilation, hypoxia in duced changes in lipid peroxidation and Na+.K+-ATPase activity progressed when nor mocapnia was reestablished. In vitro, the presence of hydroperoxides prevents the rea cylation and repair of phospholipids [17], Thus generation of free radicals during tissue hypoxia would not only alter the structure of membrane lipids by peroxidation but could also decrease the ability of the cellular repair mechanisms to restore normal membrane structure.…”

Section: Discussionmentioning

confidence: 99%

Effect of Graded Hypoxia on Brain Cell Membrane Injury in Newborn Piglets

DiGiacomo

Pane²,

Gwiazdowski³

et al. 1992

Neonatology

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Alterations in brain cell membrane structure and function during cerebral hypoxia were investigated by measuring Na⁺, K⁺-ATPase activity and levels of lipid peroxidation products in brain cell membranes obtained from newborn piglets following exposure to 60 min of hypoxic hypoxia in vivo. Cerebral hypoxia was documented as a decrease in the ratio of phosphocreatine to inorganic phosphate (PCr/Pi) using ³¹P-NMR spectroscopy. During hypoxia (FiO₂ 0.07-0.11), PCr/Pi decreased 28–47% compared to the corresponding baseline value without a decrease in cerebral ATP levels. No change in brain cell membrane Na⁺, K⁺-ATPase activity was observed for changes in PCr/Pi of < 30%. When PCr/Pi was at least 30% lower than baseline, Na⁺, K⁺-ATPase activity decreased linearly as a function of the decrease in PCr/Pi (r = 0.95). Levels of lipid peroxidation products (conjugated dienes and fluorescent compounds) increased significantly as PCr/Pi decreased. These data suggest that below a critical threshold value of oxidative metabolism there are progressive changes in brain cell membrane structure and function during cerebral hypoxia, and demonstrate that membrane alterations occur prior to changes in cellular ATP levels.

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Lipid Hydroperoxides Inhibit Reacylation of Phospholipids in Neuronal Membranes

Cited by 61 publications

References 37 publications

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Biochemical Aspects of Neurodegeneration in Human Brain: Involvement of Neural Membrane Phospholipids and Phospholipases A2

Effect of Graded Hypoxia on Brain Cell Membrane Injury in Newborn Piglets

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