Peroxidation-induced perturbations of erythrocyte lipid organization

Pradhan, Deepti; Weiser, Marybeth; Lumley-Sapanski, Katherine; Frazier, David; Kemper, Susan; Williamson, Patrick; Schlegel, Robert

doi:10.1016/0005-2736(90)90132-8

Cited by 43 publications

(29 citation statements)

References 33 publications

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“…In agreement with a number of previous studies [8][9][10], the present results clearly show that the senescent antigen is formed Erythrocytes were incubated aerobically, at 37°C, in phosphate buffer for 2 h, in the presence or in the absence of 10 mM phenylhydrazine. Iron release and methemoglobin formation were determined and the ghosts were prepared as reported in section 2.…”

Section: Discussionsupporting

confidence: 93%

“…It has been suggested that an oxidative mechanism underlies erythrocyte ageing [8,9] and it has been shown [10] that erythrocytes from vitamin E deficient rats behave like old erythrocytes from normal rats with regard to susceptibility to phagocytosis, IgG binding, anion transport ability, etc. Furthermore, increased breakdown products of band 3 were observed in membranes of erythrocytes from vit.…”

Section: Introductionmentioning

confidence: 99%

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Iron release, membrane protein oxidation and erythrocyte ageing

et al. 1995

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The aerobic incubation of erythroeytes in phosphate buffer for 24-60 h (a model of rapid in vitro ageing) induced progressive iron release and methemoglobin formation. Membrane proteins showed electrophoretic alterations and increase in carbonyl groups (as documented by IR spectroscopy). None of these phenomena were seen when the erythrocytes were incubated under anaerobic conditions. The membranes from aerobically incubated cells bound a much higher amount of autologous IgG than those from anaerobically incubated ones, suggesting that the aerobic incubation gives rise to the senescent antigen. The addition of ferrozine during the aerobic incubation prevented both the IgG binding and the protein alterations seen in the IR spectra, suggesting an intracellular chelation of the released iron by ferrozine.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Iron release, membrane protein oxidation and erythrocyte ageing

et al. 1995

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“…The significant hydrolysis by this enzyme of the membrane phospholipids PC and PE in erythrocytes previously treated with AAPH, as revealed in the present study, is therefore considered to be due to lipid bilayer perturbation effected by the AAPH radicals formed. Available evidence showing that hydrogen peroxide-treated erythrocytes became susceptible to the phagocytic action of macrophages due to loosened packing of the outer layer phospholipids of the membrane under the H2O2 attack may also support such an idea [5]. Our results showing that such an effect of 75 mM AAPH appeared even when formation of lipid peroxide was not yet observed and also that another oxidant, t-BHP, which produced abundant lipid peroxides, did not exert such an action, suggest that the observed perturbation in the membrane lipid bilayer brought by AAPH might be not due to the action of lipid peroxides secondarily formed, but rather due to the direct oxidizing action of the radical, probably on the membrane proteins.…”

Section: Discussionmentioning

confidence: 95%

“…It was already reported that exposure of erythrocytes to hydrogen peroxide, active oxygen radicals, or lipid peroxides brings about reduced activity of some membrane-bound enzymes [2,3]; opening of pores in the membrane, which permits passage of certain water-soluble, low-molecular weight substances [4]; enhanced phagocytosis by macrophages [5]; and finally hemolysis [6]. In some instances, even when lipid peroxidation by these oxidants was prevented by the addition of anti-oxidants, there still occurred some membrane damages, such as hemolysis and polymerization of certain membrane proteins [7] .…”

mentioning

confidence: 99%

Oxidative Membrane Damage and the Resulting Alteration in the Membrane Lipid Bilayer Structure of Human Erythrocytes Caused by Radical-Forming Oxidants.

Sato

Tamura

Kawaguchi

et al. 1992

J. Clin. Biochem. Nutr.

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SummaryTreatment of washed human erythrocytes for a short time (up to 2 h) with 75 or loo mlvt 2,2'-azo-bis(2-amidinopropane) dihydrochloride (AAPH), a water-soluble, radical-forming oxidant, induced considerable oxidation of the membrane protein SH groups, without any detectable formation of lipid peroxide from the membrane lipid. These cells became susceptible to the action of pancreatic phospholipase A2, and the asymmetric distribution of their membrane aminophospholipids was partially lost, accompanied by a reduced activity of the aminophospholipid translocase of the membrane. In contrast, treatment of the erythrocytes with t-butylhydroperoxide (t-BHP), a lipid-soluble, radicalforming oxidant, caused rapid and intensive lipid peroxidation, but SH oxidation to a lesser extent than that achieved by AAPH. In these cells, the membrane phospholipid asymmetry was well maintained, although the aminophospholipid translocase activity was reduced. These results suggest that AAPH might oxidize both the aminophospholipid translocase of the membrane and the membrane skeletal proteins responsible for maintenance of the asymmetric phospholipid distribution, resulting in loss of the asymmetry, and that t-BHP causes formation of peroxides from the membrane phospholipids, which might affect aminophospholipid translocase only.

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“…Lipid peroxidation of cell membranes causes a loss of the fluid properties of the membrane as well as increase in membrane permeability 23 . Lipid peroxidation products are constantly involved in some of the pathophysiological effects associated with oxidative stress in cell and tissues.…”

Section: Discussionmentioning

confidence: 99%

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2018

IJPSR

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This study evaluated the anticonvulsant effect of different extracts of Centella asiatica (CA) with particular reference to lipid metabolism in different regions of rat brain. The rats were randomly divided into 4 groups having 6 in each group: i.e. Control group received saline, PTZ-induced epileptic group (60mg/kg b.w op/ 1 day), epileptic group pretreated with chloroform extract (CE), epileptic group pretreated with aqueous (AE) extract and epileptic group pretreated with diazepam (DP; Reference control) (2 mg/kg b.w/ip/ day). The CA extract is administered at the dose of 200 mg/kg body weight orally for one week. The experimental results were observed that the decreased content of phospholipids in the entire brain regions i.e. Cerebral cortex (CC), Cerebellum (CB), Hippocampus (HC) and Pons medulla (PM); total cholesterol, triglycerides and increased content of Lipid peroxidation in epileptic rats. The reversal changes were observed on pretreatment with the chloroform extract of CA and diazepam. Hence, it is evident that the different bioactive factors of CA offered protection against PTZ-induced epilepsy.

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Peroxidation-induced perturbations of erythrocyte lipid organization

Cited by 43 publications

References 33 publications

Iron release, membrane protein oxidation and erythrocyte ageing

Iron release, membrane protein oxidation and erythrocyte ageing

Oxidative Membrane Damage and the Resulting Alteration in the Membrane Lipid Bilayer Structure of Human Erythrocytes Caused by Radical-Forming Oxidants.

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