Lipid Peroxidation Of Membrane Phospholipids Research Articles

Transcutaneous neuroadaptive electrical stimulation for treatment of uncontrolled asthma

Summary. Fifty five patients with severe uncontrolled asthma were randomly assigned to treatment with standard therapy alone (n = 25) or standard therapy combined with transcutaneous neuroadaptive electrical stimulation (n = 30). Twenty healthy volunteers were as controls. Structural and functional disorders of the erythrocyte membrane were shown to play a crucial role in the pathogenesis of severe hypoxia typical for this disease. These disorders could be due to hypoxic hyperactivity of lipid peroxidation of membrane phospholipids. The transcutaneous neuroadaptive electrical stimulation reduced severity of the cell oxidative stress, the erythrocyte membrane injury and hypoxia that resulted in improvement in clinical and functional parameters of asthma. Among the patients treated with the transcutaneous neuroadaptive electrical stimulation, good control of asthma was achieved in 17 patients (56.7 %) and partial control was achieved in 10 patients (33.3 %) compared to 13 (52 %) patients and 9 (36 %) patients, respectively, in the standard therapy group.

Lipid peroxidation of membrane phospholipids in the vertebrate retina

Retina is very rich in membranes containing polyunsaturated fatty acids. Reactive oxygen species initiates chain reactions of lipid peroxidation which injure the retina, especially the membranes that play important roles in visual function. Furthermore, biomolecules such as proteins or amino lipids can be covalently modified by lipid decomposition products. In retinal membranes, peroxidation of lipids is also usually accompanied by oxidation of membrane proteins. In consequence, lipid peroxidation may alter the arrangement of proteins in bilayers and by that interfere with their physiological role on the membrane function. Here, we review several studies on the lipid peroxidation of membrane phospholipids in retina. Particular emphasis is placed on the molecular changes of very long chain polyunsaturated fatty acids associated with protein modifications during peroxidation of photoreceptor membranes. Furthermore we use liposomes to analyze peroxidation of retinal lipids. Conjugated dienes formed from oxidized PUFAs, and TBARS products derived from the breakdown of these fatty acids located in phospholipids can be analyzed during lipid peroxidation of liposomes made of retinal lipids using Fe2+ and Fe3+ as initiators.

Lipid peroxidation contributes to age-related membrane rigidity

The aim of this work was to assess the relative contributions of lipid peroxidation and cholesterol content to the increase in membrane rigidity observed during senescence. Membrane fluidity was manipulated through exposure to peroxidized or cholesterol-loaded liposomes. Small unilamella liposomes were prepared and either peroxidized by Fe ++-ADP-ascorbic acid or loaded with cholesterol. After incorporation of the liposomes into rat liver microsomal membranes, membrane fluidity was quantitated by measuring changes in polarization. Membranes exhibited a greater sensitivity to peroxidation than cholesterol in that incorporation of peroxidized liposomes induced microsomal membrane rigidity substantially more than did cholesterol-loaded liposomes. Thus it is proposed, based on data from the present and earlier studies, that membrane fluidity can be modulated readily by lipid peroxidation of membrane phospholipids, irrespective of the influences of cholesterol. These results support the proposal that alterations of lipid structure are more potent and effective than compositional changes in cholesterol in inducing age-related increases in membrane rigidity.

Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals

Although oxygen free radicals have been implicated as mediators of cellular injury in myocardial ischemia-reperfusion, the exact nature of defects produced by these radicals is not clear. Because sarcolemmal Ca2+-pump is involved in the efflux of Ca2+ from the cell, this study was undertaken to examine the effects of oxygen free radicals on sarcolemmal ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent adenosinetriphosphatase (ATPase) activities as well as lipid peroxidation of membrane phospholipids. Isolated rat heart sarcolemmal membranes were incubated with xanthine + xanthine oxidase [a superoxide anion radical (O2-)-generating system], H2O2, or H2O2 + Fe2+ [a hydroxyl radical (HO.)-generating system] and assayed for Ca2+-pump activities. O2- inhibited the Ca2+-pump activities in a time-dependent manner; a significant inhibition of Ca2+-stimulated ATPase activity was seen after 1 min of incubation. Superoxide dismutase showed a protective effect on depression in Ca2+-pump activities caused by O2-.H2O2 inhibited Ca2+-pump activities in a dose-dependent manner; this inhibition was protected by the addition of catalase. HO. depressed the Ca2+-pump activities to a greater extent in comparison with H2O2. Mannitol showed a protective effect on HO.-induced inhibition of Ca2+-pump activities. The promotion of lipid peroxidation by free radicals was evident from increased formation of malondialdehyde. These results indicate that the sarcolemmal membrane is altered on exposure to oxygen free radicals, and this may result in depressing the Ca2+-pump mechanism for Ca2+ efflux from the myocardial cell.

Comparison of Fluorescence Characteristics of Products of Peroxidation of Membrane Phospholipids with Those of Products Derived from Reaction of Malonaldehyde with Glycine as a Model of Lipofuscin Fluorescent Substances

The fluorescence characteristics of product (I), formed during the lipid peroxidation of rat liver phosphatidylcholine liposomes containing glycine, and fluorescent product (II), derived from the reaction of malonaldehyde with glycine, were examined to elucidate the mechanism of fluorescent chromophore formation. Fluorescent product (I) had a fluorescence emission maximum at 430 nm when excited at 360 nm; its fluorescence intensity decreases in alkaline medium, but is restored by readjustment of pH to neutrality. In contrast, fluorescent product (II) exhibited an emission maximum at 458 nm, and the fluorescence was quenched at acidic pH. The fluorescent substances formed during the lipid peroxidation of hemoglobin-free human erythrocyte ghost membranes had similar fluorescence characteristics to product (I). Gel filtration experiments showed that molecular size of fluorescent product (I) was larger than that of fluorescent product (II). The thiobarbituric acid-reactive substances released from peroxidizing liposomal phospholipids had a larger molecular size than malonaldehyde, and produced little or no fluorescence with glycine. It is concluded that the precursor of the fluorescent product formed during the lipid peroxidation of membrane phospholipids differs from malonaldehyde. The mechanism of the formation of blue emitting fluorescent material, believed to be a component of lipofuscin, seems to involve peroxidized phospholipids of the membrane.

Inhibition of Ca 2+ sequestration in foetal liver microsomes by carbon tetrachloride and bromotrichloromethane

The purpose of the present work is to establish to what extent the calcium uptake of foetal liver microsomes can be modified, as in the adult, by classical hepatotoxins. The administration of liver toxins (BrCCl 3, CCl 4) to the pregnant rat or their addition to foetal and maternal liver microsome preparations causes a decrease in the level of cytochrome P-450 and a drop in the calcium storage capacity of microsomes. Lipid peroxidation of membrane phospholipids is observed in the mother but not in the foetus. On the 20th day of gestation, the foetal liver shows cytochrome P-450 dependent metabolic activity and constitutes a good model illustrating the hypothesis of calcium pump inhibition by · CCl 3 radicals without lipoperoxidation.

Effects of Dimethyl Sulphoxide and of Vitamin A on Human Platelets

SummaryDimethyl sulphoxide (DMSO) causes some release of amino acids, adenine nucleotides, and acid phosphatase and β-glucuronidase activities from washed human platelets. Addition of vitamin A with DMSO greatly enhances the effect; but vitamin A in ethanol added to platelets fails to release amino acids and nucleotides. Release appears to be due to a change in permeability of the platelet membrane, not to the discharge of contents of intracellular structures. Lipid peroxidation of membrane phospholipids, or a similar reaction, may be involved. Thrombin causes a different type of alteration in platelet permeability.The results suggest that DMSO should not be used as a preservative for platelets. They may have some bearing on the mechanisms of toxicity of DMSO and vitamin A.