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Results for “Lipid Peroxides”

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At least 19 recordsLinked to original sources
PubMed1992

Evaluation of adriamycin-induced lipid peroxidation.

Lipid peroxidation is known to be a mechanism for Adriamycin-induced toxicity. In the present study, two methods which detect fluorescent substances and high molecular weight protein aggregates in peroxidized membranes were applied to Adriamycin-induced lipid peroxidation in liver microsomes. A rat liver microsomal suspension containing an NADPH-generating system was incubated with Adriamycin. Thiobarbituric acid reactive substances (TBA-RS), formed during this incubation, were transferred from the microsomes to the medium. Fluorescent substances determined by the fluorescence emitted from both the microsomes themselves and the chloroform/methanol extracts of the microsomes, were found to be formed during this incubation. High molecular weight protein aggregates determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, were also formed. Fluorescent substances and high molecular weight protein aggregates were found in microsomal membranes themselves and increased time dependently. These substances retained in membranes can be of great use to delineate the site of Adriamycin-induced lipid peroxidation in vitro and in vivo and to determine how this lipid peroxidation affects the membrane.

Animals↗
PubMed1992

Effect of avarol and avarone on in vitro-induced microsomal lipid peroxidation.

Lipid peroxidation was employed as an experimental model to study the antioxidant properties of avarol, a sesquiterpenoid hydroquinone and of its quinone, avarone. In the NADPH- or ascorbate-linked lipid peroxidation, avarol and avarone were shown to be more effective as inhibitors than in the t-BuOOH-dependent peroxidative process. However, in all three systems employed avarol was a more powerful inhibitor than avarone. The chemical structure of avarol, having an easily donatable hydrogen atom and its kinetics of inhibition suggested that the hydroquinone acted mainly as a radical scavenger. Conversely avarone appeared to interfere mainly with the initiation phase of lipid peroxidation. However, avarol and the semiquinone intermediate may contribute to the inhibitory action of the quinone. In fact avarone reduction to avarol has been shown to occur in the presence of reducing agents such as ascorbate or Fe(II) and to be catalyzed by NADPH-supplemented microsomes.

Animals↗
PubMed1992

Ferric(III) ions inhibits copper(II)/hydrogen peroxide-catalyzing lipid peroxidation in human erythrocyte membranes.

1. Effect of ferric ions (Fe3+) on the lipid peroxidation catalyzed by copper ions (Cu2+) and hydrogen peroxide (H2O2) was studied in human erythrocyte membranes. 2. The formation of thiobarbituric acid-reactive products elicited by CuCl2/H2O2 was inhibited by FeCl3 in a concentration-dependent manner; 0.25 mM FeCl3 were enough to cause 50% inhibition of the formation of peroxides. 3. The inhibitory effect of FeCl3 is not due to competition against Cu2+. 4. FeCl3 inhibited the initiation, but did not inhibit the propagation of Cu2+/H2O2-catalyzing lipid peroxidation. 5. In the heat- or trypsin-treated erythrocyte membranes, FeCl3 had no inhibitory effect on Cu2+/H2O2-catalyzing lipid peroxidation. 6. Sodium azide, an inhibitor of catalase, had no effect on the inhibitory effect of FeCl3. 7. These results suggest that a protein factor(s), which is not catalase, is involved in the inhibition of Cu2+/H2O2-catalyzing lipid peroxidation by Fe3+.

Copper↗
PubMed1992

Red blood cell susceptibility to lipid peroxidation, membrane lipid composition, and antioxidant enzymes in continuous ambulatory peritoneal dialysis patients.

OBJECTIVE: To investigate the overall susceptibility of red blood cells (RBC) to lipid peroxidation from patients on continuous ambulatory peritoneal dialysis (CAPD). METHODS: The following parameters were measured: RBC malondialdehyde (MDA) production after oxidative stress with H2O2, RBC antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and RBC membrane lipid composition. The levels of plasma vitamin E and serum selenium were also assayed. PATIENTS: Eleven patients on continuous ambulatory peritoneal dialysis. Twenty-one healthy blood donors of similar age were used as normal controls. RESULTS: The MDA formation after H2O2 stimulation was normal in CAPD patients (0.79 +/- 0.1 mumol/gHb versus 0.78 +/- 0.1 in the control group). RBC from CAPD patients also showed a normal SOD activity, a more than adequate vitamin E status, and a peculiar pattern of membrane lipids, with reduced polyunsaturated fatty acids (p less than 0.001) and increased monounsaturated fatty acids (p less than 0.001). Both RBC GSH-Px activity, a selenium-dependent enzyme, and serum selenium levels were significantly lower in CAPD patients, and a significant positive correlation (r = 0.68; p less than 0.02) between the two parameters was found. CONCLUSIONS: This study found a normal sensitivity to oxidant stress in RBC from a group of CAPD patients, despite an impaired GSH-Px activity. The peculiar lipid pattern of RBC membrane, characterized by reduced PUFA and increased MUFA content, may contribute, in addition to adequate SOD activity and vitamin E status, to normal RBC lipid peroxidation.

Aged↗
PubMed1979

The mechanism of NADPH-dependent lipid peroxidation. The propagation of lipid peroxidation.

NADPH-dependent lipid peroxidation occurs in two distinct sequential radical steps. The first step, initiation, is the ADP-perferryl ion-catalyzed formation of low levels of lipid hydroperoxides. The second step, propagation, is the iron-catalyzed breakdown of lipid hydroperoxides formed during initiation generating reactive intermediates and products characteristic of lipid peroxidation. Propagation results in the rapid formation of thiobarbituric acid-reactive material and lipid hydroperoxides. Propagation can be catalyzed by ethylenediamine tetraacetate-chelated ferrous ion, diethylenetriamine pentaacetic acid-chelated ferrous ion, or by ferric cytochrome P-450. However, cytochrome P-450 is destroyed during propagation.

Animals↗
PubMed1992

Lipid peroxidation capacities in the myocardium of endurance-trained rats and mice in vitro.

The endurance-training programme in Experiment 1 (Exp. 1) consisted of a total swimming time of 149-159 h per male Han Wistar rat and in Experiment 2 (Exp. 2) the male NMRI-mice run on a treadmill at a speed of 25 m min-1 1 h per day, 5 days a week for 3 weeks. One group of the rat hearts was perfused with 0.3 mM cumene hydroperoxide (CumOOH) while the others were fractioned (mitochondria, sarcolemma and sarcoplasmic reticulum) and these cell fractions and homogenates were used to determine the total concentration of peroxidative lipids and the susceptibility to lipid peroxidation. The perfusion with CumOOH caused the release of thiobarbituric acid reactive substances (TBARS) into the perfusate. The release of TBARS from the trained hearts was smaller than that of the control hearts (P < 0.01). The concentration of TBARS was also smaller in the myocardium of the right ventricle of the trained rats (P < 0.01). The concentration of reduced GSH remained at a higher level after the CumOOH perfusion suggesting a better redox state in the hearts of trained animals. The concentration of the lipids susceptible to lipid peroxidation was lower in the homogenates of the trained rat hearts (P < 0.05). However, this decrease could not be explained by any of the tissue fractions used when studied in rat hearts. In Exp. 2 the total concentration of lipids susceptible to peroxidation remained unchanged in the mice hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Changes in lipid peroxidation levels and lipid composition in the lungs, livers, kidneys and brains of mice treated with paraquat.

We examined lipid peroxide levels and the lipid composition of homogenates prepared from the lungs, livers, kidneys and brains of 48 male ICR mice treated with 30 mg kg-1 paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride). The mice were divided into eight groups, in which they were killed 0, 1.5, 3, 6, 12, 24, 48 and 120 h after the administration of paraquat. A significant increase in the lipid peroxide level was identified only in the liver. Change in lipid composition was identified in all the examined organs. However, the change was not a characteristic one in which there is a selective decrease of polyunsaturated fatty acids which become degraded in a lipid peroxidation reaction. It is possible that the mechanism of paraquat toxicity may differ in different organs.

Animals↗
PubMed1979

[Lipid peroxides and atherosclerosis. The content of lipid peroxidation products in the blood in ischemic heart disease].

It was established that the content of primary (acylhydroperoxide) and secondary (intermollecular "seams" in aminophospholipids) products of lipid peroxide oxidation in blood of patients with ischemic heart disease is increased against the background of hyperlipidemia and hypercholesterolemia. It is suggested that intensification of lipid peroxide oxidation may play a role in the pathogenesis of atherosclerosis.

Adult↗
PubMed1978

Relationship between fatty acids and lipid peroxidation in lungs of neonates.

Triglycerides from the lungs of neonatal rats and mice were found to contain large amounts of the polyunsaturated fatty acids, arachidonate (20:4) and docosahexaeonoate (22:6). These fatty acids were diminished or absent in the triglycerides from the lungs of adult rats and mice and both neonatal and adult guinea pigs. No age-related changes were observed in the fatty acid composition of lung phospholipids in any of these species. The presence of arachidonic acid and docosahexaenoic acid in lung triglycerides correlated with the ability of these lungs to peroxidize lipids in vitro in all species. Depletion of lung triglycerides in neonatal rats by fasting abolished this lipid peroxidizing activity.

Age Factors↗
PubMed1992

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↗
PubMedDate not supplied

[The characteristics of the behavior and brain lipid peroxidation function of rats in acute inhalation exposure to a hydrogen sulfide-containing gas condensate].

As a result of the effect of the gas condensate containing hydrogen sulfide a depression takes place of orienting-investigatory activity of Wistar male rats in conditions of open field, disturbance of elaboration and reproduction of conditioned reflex of two-way avoidance, surplus accumulation in the cerebral cortex tissue of products of peroxide lipids oxidation and depression of catalase. The changes were of cyclic character and returned to the level of the control animals in 48 h after the finishing of the effect.

Administration, Inhalation↗
PubMed1979

Inhibition of lipid peroxidation by calcium ions and their protection of steroid hydroxylase activity from peroxidative damage.

Lipid peroxidation of adrenocortical mitochondria and microsomes was greatly stimulated by addition of 1.0 mM or less ferric ions. In the presence of NADPH-yielding system, the formation of corticosterone from endogeneous cholesterol and exogeneous deoxycorticosterone was inhibited as the concentrations of iron increased. Of interest is the fact that 0.5 mM ferric ion-mediated lipid peroxidation was completely abroagated upon addition of 2 mM calcium ions. Accordingly, protected from the peroxidative damage.

Adrenal Cortex↗
PubMed1978

Ethanol-induced hepatotoxicity; experimental observations on the role of lipid peroxidation.

Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.

Animals↗
PubMed1979

Elevation of serum lipid peroxide level associated with doxorubicin toxicity and its amelioration by [dl]-alpha-tocopheryl acetate or coenzyme Q10 in mouse (doxorubicin, toxicity, lipid peroxide, tocopherol, coenzyme Q10).

Elevations of serum lipid peroxide levels were demonstrated in mice after an equitoxic dose of doxorubicin. When BDF1 mice were injected with doxorubicin (20 mg/kg body weight, IP), lipid peroxide levels in sera were elevated 1 day after the injection and the levels declined on subsequent days. 5-Fluorouracil (400 mg/kg body weight, IP) never changed the peroxide levels in serum. Furthermore, it was found that the co-administration of [dl]-alpha-tocopheryl acetate or coenzyme Q10 IM strongly inhibited the doxorubicin-induced elevation of lipid peroxides in serum. The effectiveness of [dl]-alpha-tocopheryl acetate or coenzyme Q10 in reducing the lethality of doxorubicin in mice was also confirmed. These results indicate that the measurement of serum 2-thiobarbituric acid-reacting substances provided a useful measurement of lipid peroxide levels, which may be involved in some way with doxorubicin toxicity, and that the administration of antioxidants provide protection against some of the side effects of doxorubicin.

Animals↗
PubMed1976

Lipid peroxidation and alteration of membrane lipids in isolated hepatocytes exposed to carbon tetrachloride.

Lipid peroxidation, determined by malondialdehyde formation, occurs at a low, but detectable, rate in parenchymal cells isolated from livers of fasted rats. Pretreatment of rats with phenobarbital increased malondialdehyde formation about 2-fold, probably because of the increased amount of endoplasmic reticulum. Lipid peroxidation was increased in the cells by the addition of either NADPH or CCl4, and the effect of the two agents together was more than additive. Phenobarbital pretreatment increased peroxidation due to exposure of the cells to CCl4 but not that associated with NADPH addition. The amount of CCl4 producing a 50% increase in malondialdehyde formation was about 3-fold less for cells from phenobarbital-treated rats than for those from control rats. Decreased cytochrome P450 levels in isolated hepatocytes produced by prior treatment of rats with allylisopropylacetamide enhanced lipid peroxidation from endogenous substrates but did not affect lipid peroxidation caused by the addition of NADPH. Allylisopropylacetamide markedly lowered lipid peroxidation caused by CCl4 in proportion to the loss of cytochrome P450. Malondialdehyde production associated with metabolism of endogenous substrates in the cells, or resulting from incubation of the cells with NADPH was not accompanied by changes in the fatty acid or protein content of three membranous fractions (microsomal mitochondrial, and cell debris) isolated from homogenates of these cells. Exposure of liver cells to CCl4, however, caused major losses in all fatty acids and of protein from the microsomal fraction, but only polyunsaturated fatty acids were decreased in the cellular debris fraction. Incubation with NADPH and CCl4 together enhanced malondialdehyde formation, but caused no further decrease in fatty acid content in these two fractions. Mitochondrial fatty acids were not decreased by any treatments described.

Animals↗
PubMed1979

[Lipid peroxides and atherosclerosis. The enzymatic detoxication of lipid peroxides in the blood in ischemic heart disease due to coronary artery arteriosclerosis].

It was established that in blood of patients with ischemic heart disease due to atherosclerosis of the coronary arteries (the diagnosis was verified in selective coronaroangiography) the content of acylhydroperoxides grows while the activity of glutathione-peroxidase II decreases. In blood of patients with no damage to the coronary vessels (according to the results of angiography), glutathione-peroxidase II activity does not differ significantly from the values in the control group. The decrease of glutathione-peroxidase II activity was most marked in patients with ischemic heart disease and hypercholesterolemia. It is suggested that the increase in the peroxide content in blood of patients with ischemic heart disease may be due to the sharp decrease in the activity of glutathione-peroxidase II.

Adult↗