Alterations in mitochondrial membrane fluidity by lipid peroxidation products

Chen, Juan Juan; Yu, Byung Pal

doi:10.1016/0891-5849(94)90167-8

Cited by 334 publications

(190 citation statements)

References 41 publications

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“…43 In fatty liver, mitochondrial lipids are likely to be less protected from the attack of free radicals generated both inside and outside the organelle because of the low level of ␣-tocopherol found in the extramitochondrial space 18 and, as shown by the present study, the low GSH content in the intramitochondrial compartment. Protein damage from oxidative stress may occur either directly or as a result of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 66%

Mitochondrial Oxidative Injury and Energy Metabolism Alteration in Rat Fatty Liver: Effect of the Nutritional Status

et al. 2001

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Hepatic steatosis is associated with mitochondrial oxidative alterations. This study aimed to characterize in a choline-deficient model of rat fatty liver whether this oxidative imbalance is related to an impairment of the capacity of ATP synthesis both under fed conditions and after starvation, which may sensitize mitochondria to oxidative injury. Mitochondria were isolated from normal and fatty livers of fed or 18-hour fasted rats. Oxidative injury was evaluated by measuring the mitochondrial content of thiobarbituric reactive substances, protein carbonyls, glutathione, and protein sulfhydryls. The mitochondrial F 0 F 1 -ATP synthase content, tissue ATP concentration, and liver histology were also determined. Compared with normal liver, under fed conditions, fatty livers showed a greater mitochondrial content of oxidized lipids and proteins together with a low concentration of sulfhydryls and glutathione. The mitochondrial catalytic ␤-F 1 subunit of the F 0 F 1 -ATP synthase was about 35% lower in fatty livers. Hepatic ATP was also significantly reduced in fatty liver. Starvation exacerbated mitochondrial oxidative injury in both groups but to a greater extent in fatty livers. In the steatotic group, fasting induced a significant decrease of the ATP levels, which was accompanied by a 70% fall of the catalytic ␤-F 1 subunit. These data indicate that the mitochondrial oxidative alterations in fatty livers are associated with an important reduction of the F 0 F 1 -ATP synthase. These changes, which are greatly exacerbated after starvation, may account for the reduced synthesis of the hepatic ATP observed in the presence of fatty infiltration. (HEPATOLOGY 2001;33:808-815.)Hepatic steatosis without concomitant inflammation or fibrosis, is usually considered a benign condition. However, fatty degeneration increases the sensitivity of the liver to several types of injury, such as those due to ischemia-reperfusion 1 or drug toxicity. 2 Fatty infiltration is associated with a number of intracellular disorders, which can be either a cause or a consequence of lipid accumulation. 3 Among them, mitochondrial abnormalities related to an increased generation of reactive oxygen species have been described in human steatosis of various etiology (alcoholic 4 and nonalcoholic steatohepatitis, 5 iron, 6 or copper 7 overload) and in several experimental models of fatty liver, including alcohol administration 8 and drug toxicity. 2,9 Mitochondrial oxidative injury has been also described in conditions of chronic administration of commonly used drugs, such as valproate 10 or amiodarone, 11 the hepatic metabolites of which are known to interfere with mitochondrial respiration and fatty acid metabolism, thus producing fatty degeneration.Oxidative metabolism in mitochondria represent the main source of energy for the cells. Alterations of specific mitochondrial functions may, therefore, lead to an impaired production of ATP and a reduced uptake of substrates for mitochondrial metabolism 12 and eventually limit resistance and survival o...

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Section: Discussionmentioning

confidence: 66%

Mitochondrial Oxidative Injury and Energy Metabolism Alteration in Rat Fatty Liver: Effect of the Nutritional Status

et al. 2001

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“…35,46,47 Lipid peroxidation of membranes, a result of oxidative stress, is also known to cause changes in membrane fluidity. 48 However, lipid peroxidation produces a decrease in membrane fluidity caused by a decrease in unsaturated fatty acids 49 and/or formation of cross-linking between membrane components. 48 Although there was an increase in peroxisomal membrane fluidity, no such change was observed in other subcellular organelles (e.g., mitochondria or ER-Golgi) after LPS treatment.…”

Section: Discussionmentioning

confidence: 99%

“…48 However, lipid peroxidation produces a decrease in membrane fluidity caused by a decrease in unsaturated fatty acids 49 and/or formation of cross-linking between membrane components. 48 Although there was an increase in peroxisomal membrane fluidity, no such change was observed in other subcellular organelles (e.g., mitochondria or ER-Golgi) after LPS treatment. Therefore, the selective changes in peroxisomal membrane lipid composition may be the basis for the selective autophagy of peroxisomes in livers of animals treated with LPS.…”

Section: Discussionmentioning

confidence: 99%

Endotoxin induces structure-function alterations of rat liver peroxisomes: Kupffer cells released factors as possible modulators

et al. 2000

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We report that endotoxin treatment results in decreased amounts of peroxisomes as well as changes in structure and function of peroxisomal membranes. Peroxisomes isolated from the liver of control and treated animals showed a marked decrease in total protein, but no significant alteration in the sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) protein profile. However, the Western blot study of the peroxisomal ␤-oxidation enzymes and catalase showed an increase in those enzymes in the peroxisomal peak of normal density in endotoxin-treated rats.

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“…In addition to the chemical composition, another factor can strongly influence membrane microviscosity, namely, lipid domain peroxidation (22)(23)(24)(25)(26), and this has been the subject of several studies using FR animals.…”

Section: Studies On Membrane Microviscositymentioning

confidence: 99%

“…However, this should result in the precocious aging of animals on restricted diets, which would go against the known "anti-aging" effect of FR. Moreover, because lipid peroxidation is known as one of the major events influencing membrane microviscosity (22)(23)(24)(25)(26), the peroxidizability of cellular membranes was also investigated by using either classical methods or with the aid of a new physiological model, the measurement of mitochondrial membrane potential. The present paper presents a critical review of current problems with membrane microviscosity and lipid peroxidation in FR animals.…”

Section: Introductionmentioning

confidence: 99%

Membrane properties and lipid peroxidation in food restricted animals

Pieri

1997

AGE

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Food restriction (FR) is a well-recognized method of extending mean and maximum longevity of rodents, but the mode of its action remains to be uncovered. This article reviews the effect of FR on the physicalchemical properties and lipid peroxidizability of cellular membranes. FR prevents the age-dependent increase in microviscosity and peroxidizability of cellular membranes. It has been suggested that a decrease in the body temperature occurring in undernourished animals may play a fundamental role in the process. Indeed, the lowering of average body temperature occurring in FR animals may induce a modification in membrane lipid composition, stimulating the cells to counteract the rigidifying effect of lower temperature. Thus, membranes are maintained in a proper functional state by a mechanism similar to that found in poikilotherm animals.

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Alterations in mitochondrial membrane fluidity by lipid peroxidation products

Cited by 334 publications

References 41 publications

Mitochondrial Oxidative Injury and Energy Metabolism Alteration in Rat Fatty Liver: Effect of the Nutritional Status

Mitochondrial Oxidative Injury and Energy Metabolism Alteration in Rat Fatty Liver: Effect of the Nutritional Status

Endotoxin induces structure-function alterations of rat liver peroxisomes: Kupffer cells released factors as possible modulators

Membrane properties and lipid peroxidation in food restricted animals

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