Differential effect of lipid peroxidation on membrane fluidity as determined by electron spin resonance probes

Bruch, Richard C.; Thayer, W. S.

doi:10.1016/0005-2736(83)90525-4

Cited by 165 publications

(66 citation statements)

References 18 publications

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“…Indeed, this interpretation is supported by in vitro experiments showing that lipid peroxidation decreases membrane fluidity in artificial liposomes (6). That the observed increase in anisotropy (i.e., decrease in fluidity) oflysosomal membranes after iron loading may be due to lipid peroxidation is suggested by our observation that malondialdehyde, an end product of lipid peroxidation, was increased in hepatic lysosomal membranes isolated from iron-loaded rats.…”

Section: Discussionsupporting

confidence: 64%

“…The integrity of lysosomal membranes is essential for optimal lysosomal function, including the fusion oflysosomes with other organelles and the prevention of release of degradative lysosomal enzymes into the cell cytoplasm (2). The fluidity of lysosomal membranes is also important for lysosomal-organelle fusion and for the movement of constituents across lysosomal membranes (3)(4)(5)(6). Lysosomes normally maintain an internal pH of -4.7 via a membrane bound, proton pump (7).…”

Section: Introductionmentioning

confidence: 99%

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Alterations in the structure, physicochemical properties, and pH of hepatocyte lysosomes in experimental iron overload.

Myers

Prendergast²,

Holman³

et al. 1991

J. Clin. Invest.

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While hemochromatosis is characterized by sequestration of iron-protein complexes in hepatocyte lysosomes, little is known about the effects of excess iron on these organelles. Therefore, we studied the effects of experimental iron overload on hepatocyte lysosomal structure, physicochemical properties, and function in rats fed carbonyl iron. A sixfold increase (P < 0.0001) in hepatic iron and a fivefold increase in lysosomal iron (P < 0.01) was observed after iron loading; as a result, hepatocyte lysosomes became enlarged and misshapen. These lysosomes displayed increased (P < 0.0001) fragility, moreover, the fluidity of lysosomal membranes isolated from livers of iron-loaded rats was decreased (P < 0.0003) as measured by fluorescence polarization. Malondialdehyde, an end product of lipid peroxidation, was increased by 73% (P < 0.008) in lysosomal membranes isolated from livers of iron-overloaded rats. While amounts of several individual fatty acids in isolated lysosomal membranes were altered after iron overload, cholesterol/ phospholipid ratios, lipid/protein ratios, double-bond index, and total saturated and unsaturated fatty acids remained unchanged. The pH of lysosomes in hepatocytes isolated from livers of iron-loaded rats and measured by digitized video microscopy was increased (control, 4.70±0.05; iron overload, 5.21 ±0.10; P < 0.01). Our results demonstrate that experimental iron overload causes marked alterations in hepatocyte lysosomal morphology, an increase in lysosomal membrane fragility, a decrease in lysosomal membrane fluidity, and an increase in intralysosomal pH. Iron-catalyzed lipid peroxidation is likely the mechanism of these structural, physicochemical, and functional disturbances. (J. Clin. Invest. 1991. 88:1207-1215

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Alterations in the structure, physicochemical properties, and pH of hepatocyte lysosomes in experimental iron overload.

Myers

Prendergast²,

Holman³

et al. 1991

J. Clin. Invest.

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show abstract

“…In line with these data, it has been already reported that the main effect of peroxidation on lipid dynamics and membrane order is a general decrease of the membrane fluidity. 49,50 Moreover, here we demonstrate that membrane affinity of LOX-1 in the presence of calcium ions is almost doubled when membranes contain AEA or 2-AG. This observation suggests a preferential interaction of LOX-1 with eCBs-containing membranes, that in vivo could contribute to the different subcellular localization of the enzyme.…”

Section: ■ Concluding Remarkssupporting

confidence: 57%

Impact of Embedded Endocannabinoids and Their Oxygenation by Lipoxygenase on Membrane Properties

Dainese

Sabatucci

Angelucci

et al. 2012

ACS Chem. Neurosci.

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N-Arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol are the best characterized endocannabinoids. Their biological activity is subjected to metabolic control whereby a dynamic equilibrium among biosynthetic, catabolic, and oxidative pathways drives their intracellular concentrations. In particular, lipoxygenases can generate hydroperoxy derivatives of endocannabinoids, endowed with distinct activities within cells. The in vivo interaction between lipoxygenases and endocannabinoids is likely to occur within cell membranes; thus, we sought to ascertain whether a prototypical enzyme like soybean (Glycine max) 15-lipoxygenase-1 is able to oxygenate endocannabinoids embedded in synthetic vesicles and how these substances could affect the binding ability of the enzyme to different lipid bilayers. We show that (i) embedded endocannabinoids increase membrane fluidity; (ii) 15-lipoxygenase-1 preferentially binds to endocannabinoid-containing bilayers; and that (iii) 15-lipoxygenase-1 oxidizes embedded endocannabinoids and thus reduces fluidity and local hydration of membrane lipids. Together, the present findings reveal further complexity in the regulation of endocannabinoid signaling within the central nervous system, disclosing novel control by oxidative pathways.

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“…Many researchers reported that membrane fluidities were decreased by the peroxidation of phospholipid vesicles, erythrocytes, microsomes, and mitochondrial membranes [85][86][87][88][89][90][91], whereas Grzelinska et al [92] showed increased membrane fluidity following peroxidation of erythrocytes membrane. We [93] observed that heart sarcolemmal, sarcoplasic reticular, and mitochondrial membrane fluidities were decreased by 2 mM xanthine plus 0.03 U/ml xanthine oxidase during 5 to 30 min of incubation.…”

Section: Membrane Permeability Membrane Fluidity and Phosphatidyletmentioning

confidence: 99%

Oxygen free radicals and calcium homeostasis in the heart

et al. 1994

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Many experiments have been done to clarify the effects of oxygen free radicals on Ca 2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analyze the results.It is, however, evident that Ca 2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca 2+ binding is increased, Ca 2+ influx through Ca 2 § channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca 2. can enter the myocytes is Na+-Ca 2+ exchanger. Although, the activities ofNa § + ATPase and Na+-H + exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na § level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na § Ca z+ exchange in Ca 2+ influx process from extracellular space. Another question is 'which way does Na+-Ca 2+ exchange work under oxidative stress? Net influx or efflux of Ca 2 § ?' Membrane permeability for Ca 2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pumpATPase activity is depressed by oxygen free radicals, Ca 2 § extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca 2 § release from sarcoplasmic reticulum and inhibit Ca 2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca 2+ handling systems could cause the Ca 2+ overload due to oxygen free radicals. (Mol Cell Biochem 139: 91-100, 1994)

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Differential effect of lipid peroxidation on membrane fluidity as determined by electron spin resonance probes

Cited by 165 publications

References 18 publications

Alterations in the structure, physicochemical properties, and pH of hepatocyte lysosomes in experimental iron overload.

Alterations in the structure, physicochemical properties, and pH of hepatocyte lysosomes in experimental iron overload.

Impact of Embedded Endocannabinoids and Their Oxygenation by Lipoxygenase on Membrane Properties

Oxygen free radicals and calcium homeostasis in the heart

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