[Studies on serum lipid peroxides. 2. Observation on serum lipid peroxides and alpha-tocopherol in acute apoplexy].
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Acute Disease↗
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Effects of vitamin E-enriched egg yolk on lipid peroxidation, hemolysis and serum lipid concentration in young and old rats.
Effects of a diet containing different amount of vitamin E-enriched egg yolk powder on lipid peroxidation, hemolysis, and serum lipid concentration were examined in young and old rats. Young and old rats were fed experimental diets containing 5.6% or 22.5% of normal egg yolk powder, and 5.6% or 22.5% of vitamin E-enriched egg yolk powder. When young rats were fed these diets, their tocopherol concentrations in testes, heart, kidneys, and retroperitoneum fat pads increased according to the diet tocopherol contents. Lipid peroxide levels in these tissues were inversely proportional to the tocopherol concentrations. The liver and serum, however, did not show the above relationship. In the rats fed vitamin E-enriched egg yolk diets hemolysis did not increase, in contrast to those fed normal egg yolk diets. The rats fed a 5.6% vitamin E-enriched egg yolk diet had a lower serum cholesterol level than those fed a normal egg yolk diet. In old rats, one control group was used to determine initial tocopherol concentration and two other groups were fed 5.6% normal and vitamin E-enriched egg yolk diets. The vitamin E-enriched egg yolk rats showed lower weights of the body, liver, and retroperitoneum fat pads at the end of the experiment. The normal egg yolk group had atrophied testes. The tissue and serum tocopherol concentrations were increased in the vitamin E-enriched egg yolk group, whereas they were decreased in the normal egg yolk group. In the vitamin E-enriched egg yolk group, lipid peroxide, hemolysis and serum cholesterol, especially HDL-cholesterol, did not increase. These results indicate that egg yolk tocopherol was absorbed and prevented lipid peroxidation and hemolysis in young and old rats, and testes atrophy in old rats.
Age Factors↗
2'-deoxycytidine in free nucleosides and double-stranded DNA as the major target of lipid peroxidation products.
Lipid peroxidation generates a variety of reactive products that covalently modify DNA, yielding several types of adducts with nucleobases. In the present study, we characterized the modification of nucleobases during peroxidation of linoleate and found that 2'-deoxycytidine (dC) could be a major target of the modification by lipid peroxidation reactions. Upon incubation with oxidized linoleate, dC and 2'-deoxyguanosine (dG) were significantly modified among four 2'-deoxynucleosides. The major product in dG/linoleate was identical to the 2-oxo-heptyl-substituted 1,N(2)-etheno-dG that had been previously identified as a 4-oxo-2-nonenal (ONE)-dG adduct. On the basis of spectroscopic and chemical characterization, we identified the major product in dC/linoleate as the 2-oxo-heptyl-substituted 3,N(4)-etheno-dC. The same adduct was also produced upon reaction of dC with ONE, suggesting that ONE might represent the major reactive species that modifies DNA during lipid peroxidation. Indeed, this proposition was supported by the observation that ONE was far more reactive with dC and dG than other genotoxic aldehydes, such as 4-hydroxy-2-nonenal. More strikingly, we found that, in contrast to the similar reactivity of ONE toward free nucleobases (dC and dG), ONE preferentially reacted with dC residues in double-stranded DNA. These results suggest that ONE and other 4-oxo-2-alkenals may possess by far the strongest electrophilic potential vs. dC and that the formation of 4-oxo-2-alkenal-adducted dC may thus serve as one mechanism for oxidative damage to DNA in vivo.
Aldehydes↗
[The interconnection of changes in the level of prostaglandins, catecholamines, and lipid peroxidation of membrane lipids in patients with bronchial asthma].
Dynamics of alterations in content of prostaglandins (PG) F2 alpha and E and in the ratio PGF2 alpha/PGE was studied in blood plasma of 24 patients with chronic asthmatic bronchitis and 109 patients with bronchial asthma. Alterations in content of PGF2 alpha correlated with severity of the disease, while PGE content was similarly below the control values in all the groups examined. The ratio PGF2 alpha/PGE corresponded with the alterations in content of PGF2 alpha. Direct correlation was observed between content of adrenaline, PGF2 alpha and the rate of lipid peroxidation, whereas PGE was not related to these patterns. The correlation was completely absent under conditions of asthmatic attack.
Adult↗
Paraquat and ferritin-dependent lipid peroxidation.
A lipid peroxidation system consisting of phospholipid liposomes, paraquat, ADP, and NADPH-cytochrome P450 reductase was constituted using ferritin as the sole source of iron. Lipid peroxidation was completely inhibited by superoxide dismutase, essentially not affected by mannitol, but markedly stimulated by catalase. Similar effects of these scavenging agents were observed in incubations void of ADP. These data suggest that O2-, produced by the redox cycling of paraquat, can release iron from ferritin and thereby promote lipid peroxidation. The effects of catalase and mannitol suggest that the initiation of peroxidation, in either the presence or absence of ADP, is not significantly dependent upon the hydroxyl radical produced via an iron-catalyzed Haber-Weiss reaction.
Adenosine Diphosphate↗
A high involvement of O2- possibly generated in inner membranes for iron-induced microsomal lipid peroxidation.
The lipid peroxidation of and the O2- generation by rat liver microsomes in the presence of NADPH or both NADPH and Fe3+ were determined by thiobarbituric acid-reacting substance formation and by chemiluminescence intensities with a cypridina luciferin analog, 2-methyl-6-(p-methoxyphenyl)-3, 7-dihydroimidazo[1,2-a]pyrazin-3-one(MCLA), as a chemiluminescence probe. Judging from the experiments with various inhibitors on the O2- generation and the lipid peroxidation, O2- generated, at intramembranous site, by cytochrome P-450 system is considered to be highly involved in the iron-induced lipid peroxidation.
Animals↗
In vivo hemoglobin dosimetry of malonaldehyde and ethene in mice after induction of lipid peroxidation. Effects of membrane lipid fatty acid composition.
Hemoglobin (Hb) adduct determination by the N-alkyl Edman method was used for in vivo dosimetry of endogenously formed malonaldehyde (MA) and ethene in mice fed diets with different fatty acid composition and induced for lipid peroxidation with carbon tetrachloride (CCl4). In order to amplify lipid peroxidation animals were pretreated with phenobarbital (PB) and the glutathione-depleting agent DL-buthionine-(S,R)-sulfoximine (BSO). Non-treated animals raised on different diets were used as controls. Lipid peroxidation products in liver were measured as 2-thiobarbituric acid reactive compounds (TBA-C). Livers from control mice fed a soya oil based diet (rich in polyunsaturated fatty acids, diet S) showed approximately 6.5-fold higher levels of TBA-C than those from animals raised on a coconut oil based diet (mostly saturated fatty acids, diet C). The level of adducts of MA to Hb, determined as N-(3-hydroxypropyl)valine, was approximately 1.5-fold higher in animals from diet S than in animals raised on diet C. The highest increases in the levels of TBA-C and MA adducts were obtained after a simultaneous treatment of the animals with PB, BSO and CCl4. The increases of TBA-C were 1.3-fold (diet C) and 1.7-fold (diet S). The corresponding increases of MA-Hb adduct levels were 1.3- and 1.6-fold respectively, indicating an increased susceptibility of mice fed diet S to lipid peroxidation. The level of adducts from ethene, determined as N-(2-hydroxyethyl)valine, was also higher in mice from diet S than in animals fed diet C, when all treatment groups were considered. The difference was, however, only slightly significant (P less than 0.02). No difference between control and CCl4-treated animals, with regard to the ethene-Hb adduct, was found. Our results validate the use of Hb dosimetry for monitoring the effects of factors known to influence lipid peroxidation induced in vivo.
Animals↗
Attenuation of lipid peroxidation by antioxidants in rat-1 fibroblasts: comparison of the lipid peroxidation reporter molecules cis-parinaric acid and C11-BODIPY(581/591) in a biological setting.
Lipid peroxidation is a major factor in the pathogenesis of many disease states. To detect the initial stages of lipid peroxidation or evaluate antioxidant efficacy, cis-parinaric acid (cis-PnA) has been successfully used and thoroughly validated. However, cis-PnA is not very well suited for medium throughput screening of antioxidants in living cells. We recently introduced and validated a lipid peroxidation reporter molecule, C11-BODIPY(581/591). To further explore this probe, we evaluated the protective effect of 12 natural antioxidants in rat-1 fibroblasts subjected to 50 microM cumene-hydroperoxide using both probes. The same pecking order for the individual antioxidant efficacies was obtained: alpha-tocopherol approximately gamma-tocopherol > quercetin approximately lycopene > kaempferol > palm oil > hydroxy-tyrosol > > alpha-carotene = beta-carotene = lutein = tyrosol = chlorogenic acid. This validates the accuracy of the C11-BODIPY(581/591) method and shows that this assay is an accurate and highly flexible method for indexing lipid peroxidation or determining antioxidant efficacy in living cells in a medium throughput scenario. The antioxidant efficacy was compared with their one-electron reduction potential, hydrophobicity and Trolox C equivalent antioxidant capacity. Our results show that although these parameters are valuable for determining structure-function relationships, they have limited predictive value for antioxidant efficacy in vivo.
Animals↗
Rabbit liver microsomal lipid peroxidation. The effect of lipid on the rate of peroxidation.
Rat and rabbit liver microsomes catalyze an NADPH-cytochrome P-450 reductase-dependent peroxidation of endogenous lipid in the presence of the chelate, ADP-Fe3+. Although liver microsomes from both species contain comparable levels of NADPH-cytochrome P-450 reductase and cytochrome P-450, the rate of lipid peroxidation (assayed by malondialdehyde and lipid hydroperoxide formation) catalyzed by rabbit liver microsomes is only about 40% of that catalyzed by rat liver microsomes. Microsomal lipid peroxidation was reconstituted with liposomes made from extracted microsomal lipid and purified protease-solubilized NADPH-cytochrome P-450 reductase from both rat and rabbit liver microsomes. The results demonstrated that the lower rates of lipid peroxidation catalyzed by rabbit liver microsomes could not be attributed to the specific activity of the reductase. Microsomal lipid from rabbit liver was found to be much less susceptible to lipid peroxidation. This was due to the lower polyunsaturated fatty acid content rather than the presence of antioxidants in rabbit liver microsomal lipid. Gas-liquid chromatographic analysis of fatty acids lost during microsomal lipid peroxidation revealed that the degree of fatty acid unsaturation correlated well with rates of lipid peroxidation.
Adenosine Diphosphate↗
Autoxidation of rat brain homogenate: evidence for spontaneous lipid peroxidation. Comparison with the characteristics of Fe2+- and ascorbic acid-stimulated lipid peroxidation.
Aerobically-incubated brain homogenates are known to undergo autoxidation characterized by spontaneous TBARS production, presumably as a result of lipid peroxidation. However, TBARS measurement alone, because of its lack of specificity, is not sufficient to demonstrate the occurrence of lipid peroxidation in complex biological systems. This study, undertaken to determine whether or not spontaneous oxidation of rat brain homogenate is due to lipid peroxidation, measured different specific markers of this process (fatty acids, lipid aldehydes and the formation of fluorescence products) and studied changes in alpha-tocopherol. Incubation of rat brain homogenates at 37 degrees C under air led to spontaneous TBARS formation, which was accompanied by lipid aldehydes and lipid fluorescence products as well as polyunsaturated fatty acid (PUFA) degradation. Alpha-tocopherol was also consumed. On the whole, these results demonstrate that autoxidation of brain homogenate is a spontaneous lipid peroxidation process. When homogenates were exposed to Fe2+ and ascorbic acid-induced oxidative stress, lipid peroxidation was enhanced. However, spontaneous and stimulated peroxidation showed similar patterns not characteristic of classical lipid peroxidation, i.e. without the lag and accelerating phases typical of a propagating chain reaction. PUFA degradation was limited despite stimulation of peroxidation.
Animals↗
Extracellular calcium alleviates cell toxicity due to hepatotoxins that induce lipid peroxidation, but has no effect on toxins that do not cause lipid peroxidation. A study in isolated rat hepatocytes.
The effect of extracellular calcium on cell death, induced by hepatotoxins that induce lipid peroxidation [diethyl maleate (DEM), allyl alcohol (AA) and bromoisovalerylurea (BIU)] and hepatotoxins that do not induce lipid peroxidation [disulfiram (DSF), N-hydroxy-2-acetyl-aminofluorene (N-OH-AAF) and tetrahydroaminoacridine (THA)] was studied in freshly isolated rat hepatocytes. Extracellular calcium strongly delayed the onset of toxicity of DEM, AA and BIU as detected by lipid peroxidation, depletion of free protein thiol groups and cell death. This protective effect of calcium was decreased at higher concentrations of the toxic compounds. In contrast, no effect of calcium was observed on toxicity induced in the absence of lipid peroxidation by DSF, N-OH-AAF and THA. Addition of calcium was also without effect on the protein thiol depletion. These results indicate that calcium only alleviates cytotoxicity which is induced by thiol depletion resulting from lipid peroxidation. Cytotoxicity as a result of protein thiol depletion through disulfide formation is not affected by extracellular calcium.
1-Propanol↗
[Changes in the lipid and protein components of thymus cell membrane during lipid peroxidation].
Nonenzymatic lipid peroxidation in thymus cell plasma membranes was studied. The composition of lipid and protein components, intensity of fluorescence of the membrane probes (1-anilinonaphthalene-8-sulfonate, 4-dimethylaminochalcon, eosin, pyronin and rhodamine), fluorescence polarization of tryptophan residues of membrane proteins and quenching by acrylamide of intrinsic fluorescence of proteins were determined. Induction of lipid peroxidation by the Fe(2+)-ascorbate system caused changes in the composition and structure of lipids. This was paralleled with changes in the structural-dynamic organization of membrane proteins, transition of some peripheral proteins to the water phase and increased solubilization of integral proteins by Triton X-100.
Animals↗
Inverse regulation of lipid-peroxidizing and hydroperoxyl lipid-reducing enzymes by interleukins 4 and 13.
12/15-lipoxygenases and phospholipid hydroperoxide glutathione peroxidases are opposite enzymes balancing the intracellular concentration of hydroperoxy lipids. We studied the regulation of both enzymes by interleukins 4 and 13 and found an inverse response. When human lung carcinoma cells A549 were cultured in vitro in the presence of these cytokines, an up-regulation of the 12/15-lipoxygenase and a down-regulation of the phospholipid hydroperoxide glutathione peroxidase were observed. A similar inverse regulation was found in human peripheral monocytes. Interleukin 4-treated A549 cells exhibited an impaired capability of reducing exogenous hydroperoxyl lipids and their levels of endogenous lipid hydroperoxides were markedly increased. To find out whether these regulatory processes also occur in vivo, arachidonic acid oxygenase and phospholipid hydroperoxide glutathione peroxidase activity was assayed in various tissues of transgenic mice that systemically overexpress interleukin 4. In lung, spleen, kidney, and heart, an increased arachidonic acid oxygenase activity was detected when transgenic mice were compared with inbred controls. The phospholipid hydroperoxide glutathione peroxidase activity was impaired in lung, liver, and spleen of the transgenic animals. These data indicate that lipid-peroxidizing and lipid peroxide-reducing enzymes are inversely regulated in various mammalian cells. Up-regulation of the 12/15-lipoxygenase and simultaneous down-regulation of the phospholipid hydroperoxide glutathione peroxidase may lead to an increased oxidizing potential, which is reflected by an augmented intracellular peroxide tone.
Animals↗
Effects of paraquat on peroxide metabolism enzymes and lipid peroxidation in the rat.
Investigation has been made of how the LD50 and LD100 of PQ influence the peroxide metabolism enzymes and lipid peroxidation in organ homogenates and blood samples of the rat. The peroxide metabolism enzyme activities were changed in a concentration dependent manner. In general, the effect of the lower doses of PQ on the superoxide dismutase, catalase activities and lipid peroxidation are increased. The glutathione peroxidase activity was decreased. Higher doses of PQ enhanced all of enzyme activities and lipid peroxidation studied.
Animals↗
Detection of lipid peroxidation products in lipids and tissues by gas chromatography-mass spectrometry.
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Animals↗
Lipid peroxides in obese patients and effects of weight loss with orlistat on lipid peroxides levels.
OBJECTIVE: Obesity is a well-known risk factor of atherosclerosis. Recent studies showed that obesity is associated with enhanced lipid peroxidation. The aim of this study is to investigate the effect of weight reduction with orlistat treatment on lipid peroxidation levels. We assessed lipid peroxidation by measuring the concentration of plasma malondialdehyde (MDA). DESIGN: A randomized, controlled, open-label 6-month study. SUBJECTS: In total, 36 obese (body mass index (BMI) >30 kg/m2) and 11 healthy age-matched control subjects were enrolled in the study. MEASUREMENTS: Fasting glucose, triglyceride, total cholesterol, HDL cholesterol and LDL cholesterol and MDA levels were measured in both groups. Obese subjects received orlistat, 120 mg three times daily together with hypocaloric diet. After 6 months of treatment laboratory tests were repeated. RESULTS: MDA levels were significantly higher in obese patients than the control group (P<0.0001). After 6 months of treatment in obese subjects, the mean weight of the patients decreased by 6.8 kg, the BMI by 3.2 kg/m2. Plasma MDA levels were significantly reduced by weight loss from 2+/-0.77 to 0.89+/-0.41 nmol/ml (P<0.001). BMI correlated with MDA levels at baseline (r=0.6, P<0.0001). Changes in BMI was positively associated with plasma MDA level reduction (r=0.36, P<0.05). CONCLUSION: These results indicate that obesity is associated with increases in endogenous lipid peroxides. Our data show that the indicator of lipid peroxidation-MDA-falls markedly in association with weight loss with orlistat. The demonstration of decreased free radical generation has important implications for oxidative mechanism underlying obesity-associated disorders.
Adult↗
Red wine polyphenolic compounds inhibit atherosclerosis in apolipoprotein E-deficient mice independently of effects on lipid peroxidation.
BACKGROUND: Lipid peroxidation is thought to play an important role in the pathogenesis of atherosclerosis. Fatty acid peroxidation products such as hydroxyeicosatetraenoic acids and F(2)-isoprostanes have been found in advanced human atherosclerotic plaques. However, little is known about the formation of these products during lesion development. OBJECTIVE: This study examined stable biomarkers of lipid oxidative damage in relation to atherosclerotic disease progression in apolipoprotein E-deficient (Apoe(-/-)) mice and retardation of the disease by red wine polyphenols. DESIGN: One hundred male Apoe(-/-) mice and 50 male control (C57BL/6J) mice were given a high-fat, high-cholesterol diet for 20 wk. To examine the effect of the polyphenolic compounds on lesion development, 50 of the Apoe(-/-) mice were also given dealcoholized red wine for the duration of the study. RESULTS: Aortic lipid deposition was significantly greater in the Apoe(-/-) mice than in the control mice (P < 0.01). Plasma and aortic F(2)-isoprostanes did not differ between the treatment groups. Plasma concentrations of monocyte chemoattractant protein 1, which has been implicated in the development of atherosclerosis, were significantly higher in the Apoe(-/-) mice than in the control mice up to 16 wk (P < 0.05). Hydroxyeicosatetraenoic acid concentrations increased significantly over time in all groups (P < 0.05). Red wine polyphenols had no effect on markers of lipid peroxidation or monocyte chemoattractant protein 1 concentrations, but lipid deposition in the aorta at age 26 wk was significantly less in the mice given red wine than in those not given red wine. CONCLUSION: These results suggest that lipid deposition is independent of lipid oxidation and that the protective action of red wine polyphenols is independent of any antioxidant action of these compounds.
Animals↗
Effect of succinate on mitochondrial lipid peroxidation. 2. The protective effect of succinate against functional and structural changes induced by lipid peroxidation.
The damaging effects of ADP/Fe/NADPH-induced lipid peroxidation were studied on the enzymes and membranes of rat liver mitochondria. Succinate, an inhibitor of mitochondrial lipid peroxidation, prevented or delayed most of the damage caused by the peroxidation on different mitochondrial structures and functions. There were marked abnormalities on the electrophoretic pattern of mitochondrial proteins during the course of lipid peroxidation. The disappearance of particular polypeptide bands and the accumulation of high-molecular-weight aggregates could be observed. Succinate was found to delay these effects. As a consequence of lipid peroxidation the succinate oxidase activity of mitochondria was decreased. The succinate dehydrogenase enzyme and the component(s) of the respiratory chain were inactivated. Succinate prevented the inactivation of succinate dehydrogenase but did not protect the other components of terminal oxidation chain. From the matrix enzymes the glutamate dehydrogenase retained its full activity but the NADP-linked isocitrate dehydrogenase was inactivated. The mitochondrial membranes became permeable to large protein molecules. Succinate prevented the inactivation of isocitrate dehydrogenase and delayed the release of protein molecules from mitochondria.
Animals↗