The increase of phospholipid bilayer rigidity after lipid peroxidation

Dobretsov, G. E.; Borschevskaya, T.A.; Петров, В. А.; Vladimirov, Yu. A.

doi:10.1016/0014-5793(77)81071-5

Cited by 277 publications

(105 citation statements)

References 16 publications

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“…Alterations in membrane fluidity by the action of ionizing radiation have been reported in several studies. Radiation induced rigidization of membrane observed can be attributed to the radiation initiated radical generation and subsequent reactions with lipid molecules of the membranes, producing peroxidation and crosslinking of membrane components by peroxidative products [15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Interfacial properties as predictors of radioresistance in cervical cancer

Anand

Huilgol

Banerjee

2007

Journal of Colloid and Interface Science

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Section: Discussionmentioning

confidence: 99%

Interfacial properties as predictors of radioresistance in cervical cancer

Anand

Huilgol

Banerjee

2007

Journal of Colloid and Interface Science

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“…Membranes damaged by peroxidation of the polyunsaturated fatty acids by aging, ozone, or chemical oxidizing agents show marked increases in the temperature at which this change in molecular ordering occurs (4,20,21). Concomitant with this change in molecular ordering are marked decreases in the fluidity of the membrane (7,9), increases in the ratio of saturated to unsaturated fatty acids (9,21), and increases in the permeability of the membrane (11,19).…”

Section: Discussionmentioning

confidence: 99%

Changes in Tobacco Cell Membrane Composition and Structure Caused by Cercosporin

Daub

Briggs²

1983

Plant Physiol.

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Cercosporin, a toxin produced by Cercospora species, rapidly kills plant cells in the Light. Previous work has shown that cercosporin treatment causes products of lipid peroxidation to be released. We have found that the unsaturated acyl chains of lipids in tobacco (Niotiana tabacum) cell membranes are destroyed when cells are treated with cercosporin. Concomitant with this change in composition is a change in structure of the membranes as detected by two different fatty acid spin labels, 2-(3-carboxypropyl)4,4-dimethyl-2-tridecyl-3-oxazolidinyloxyl (denoted 1112,31) and 2-(1'-carboxytetradecyl)-2-ethyl-4,4-dmethyl-3-oxazolidinyloxyl (denoted 111,141). Cercosporin causes the membranes to become more rigid at all temperatures tested and increases the membrane phase transformation temperature from 12.70C to 20.80C.Cercosporin, a toxic compound from Cercospora species, affects both hosts and non-hosts of the producing fungi. Cercosporin was first isolated in 1957 by Kuyama and Tamura (14) from C. kikuchii, a soybean pathogen, and has since been isolated from a large number of Cercospora species (1,8,16) and from Cercosporainfected plants (8,14). The structure of cercosporin was determined independently by Lousberg et al. (15) and Yamazaki and Ogawa (25).Cercosporin is a photosensitizing agent capable of generating both singlet oxygen and superoxide during irradiation (M. Daub and R. Hangarter, unpublished). Plant cells, bacteria, and mice are killed rapidly by cercosporin in the presence of light (5,26). Cercosporin causes electrolytes to leak from plant tissues (6, 17), destroys plant protoplasts (6), and causes peroxidation of plant membrane lipids both in vitro (3) and in vivo (6). These data suggest that cercosporin acts directly on membranes in situ.We report here that cercosporin causes a large increase in the ratio of saturated to unsaturated fatty acids extracted from membranes of toxin-treated cells. Concomitant with this change is a decreased membrane fluidity and the possible appearance of a phase separation in the membranes at the growth temperature of the cells. Electrolyte leakage and cell death may be accounted for by these perturbations of membrane composition and structure. MATERIALS AND METHODS Cercosporin. Cercosporin was isolated and purified from cultures of Cercospora nicotianae as previously described (5). Stock solutions were prepared in acetone and stored at -20°C in the dark. Control cultures were either treated with the same concentration of acetone or treated with cercosporin but incubated in the dark. Final acetone concentrations in both treated and control cultures did not exceed 1% (v/v).Host Material. All experiments were conducted with Nicotiana tabacum cv. 'Wisconsin 38' cell culture line NT575. Liquid suspension cultures were maintained as previously described (5).Protoplast Isolation. Protoplasts were isolated from NT575 suspension cultures 2 d after subculture (early log phase). The cells were preplasmolyzed in 0.6 M mannitol for 2 h followed by centrifugation. Packed ...

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“…Furthermore, higher unsaturated fatty acid content may make these cells more susceptible to lipid peroxidation. The return to more normal fluidity values with ascorbate treatment may occur because of ascorbate-mediated peroxidation (16,31) rather than from a "correction" of a basic membrane defect . That such normalization is important to the cell's function is suggested by the improved chemotaxis of CHS PMN treated with ascorbate (5) .…”

Section: Discussionmentioning

confidence: 99%

Fluidity properties and liquid composition of erythrocyte membranes in Chediak-Higashi syndrome.

Ingraham

Burns

Boxer

et al. 1981

The Journal of Cell Biology

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We have earlier shown through electron spin resonance (ESR) studies of leukocytes that membranes of cells from both Chediak-Higashi syndrome (CHS) mice and humans have abnormally high fluidity . We have extended our studies to erythrocytes . Erythrocytes were labeled with the nitroxide-substituted analogue of stearic acid, 2-(3-carboxypropyl)-4,4-dimethyl-2-tridecyl-3-oxazolidinyloxyl, and ESR spectra were obtained . Order parameter, S, at 23°C, was 0.661 and 0.653 for erythrocytes of normal and CHS mice (P < 0.001) . S was 0.684 for normal human erythrocytes and 0.675 (P < 0.001) for CHS erythrocytes at 25°C. Because S varies inversely to fluidity, these results indicate that CHS erythrocytes tend to have higher fluidity than normal . In vitro treatment of both mice and human CHS erythrocytes with 10 mM ascorbate returned their membrane fluidity to normal . We prepared erythrocyte ghosts and extracted them with CHC1 3:CH3OH (2 :1) . Gas-liquid chromatography analysis showed a greater number of unsaturated fatty acids for CHS . The average number of double bonds detected in fatty acids for mice on a standard diet was 1 .77 for normal and 2.02 for CHS (P < 0.04) ; comparison of human erythrocytes from one normal control and one CHS patient showed a similar trend . Our results suggest that an increased proportion of unsaturated fatty acids may contribute to increased fluidity of CHS erythrocytes . Our observation that both leukocytes and erythrocytes of CHS have abnormal fluidity indicates that CHS pathophysiology may relate to a general membrane disorder.

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The increase of phospholipid bilayer rigidity after lipid peroxidation

Cited by 277 publications

References 16 publications

Interfacial properties as predictors of radioresistance in cervical cancer

Interfacial properties as predictors of radioresistance in cervical cancer

Changes in Tobacco Cell Membrane Composition and Structure Caused by Cercosporin

Fluidity properties and liquid composition of erythrocyte membranes in Chediak-Higashi syndrome.

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