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PubMedDate not supplied

Age-dependent production of mitochondrial hydrogen peroxide, lipid peroxides and fluorescent pigments in the rat heart.

Mitochondria were prepared from hearts of 3-, 14-, 18-, and 24-month-old male Wistar rats. Respiratory control ratio (RCR) values did not change with age in the glutamate or succinate-induced respiration except at 24 months in which RCR values significantly increased with both the substrates. Using still glutamate or succinate as substrates the production of H2O2 was measured in the presence of antimycin. A 70% and 25% increase in H2O2 formation was observed at 14 and 18 months of age, respectively, in comparison to the youngest group. Only in the presence of succinate was a 25% elevation in H2O2 found at 24 months of age. These observations parallel with the decrease of the ratio between tissue levels of reduced and oxidized glutathione that was observed at 14 and 18 months of age. The concentration of myocardial malondialdehyde, a secondary product of lipid peroxidation, remained the same at all ages measured, most probably because it is readily metabolized in vivo. On the contrary the myocardial level of lipofuscin, which is not degraded by the cell, progressively increased beginning from 18 months of age.

Aging↗
PubMed1987

Lipid peroxidation and lipid peroxide detected by chemiluminescence.

This article emphasizes the advantages of using a luminescence spectrometer based on photon counting techniques for the detection of lipid peroxidation. An overview is presented of how chemiluminescence can be stimulated in the luminol-cytochrome c heme peptide system as an assay for lipid hydroperoxides. This method is used for finding antioxidant drugs. The specificity and advantages of the chemiluminescent method for detecting lipid hydroperoxides is reviewed.

Animals↗
PubMed1991

Effects of taurine and ketamine on bovine retinal membrane lipid peroxidation.

Lipid peroxidation disrupts membrane integrity and causes structural and functional alterations in ischemic tissues. Taurine and ketamine are putative ischemic protectants that affect Ca2+ influx. Here we report the influence of these compounds on lipid peroxidation in subcellular fractions, isolated cells and intact tissue from bovine retinas. P2 membrane fractions and isolated cells were exposed to the lipid peroxidation inducers cadmium chloride (200 microM) or L-ascorbic acid (1 mM) in the presence of 0-50 mM taurine, 0-10 mM ketamine, 1 mM kynurenic acid or 1 mM dextromethorphan. The latter compounds are N-methyl-D-aspartate receptor antagonists. Lipid peroxidation in isolated eyes reperfused after 1 h of ischemia either with or without protectants was determined by thiobarbituric acid assay. Glutathione was measured in isolated retinas subjected in vitro to simulated ischemia (no glucose or oxygenation) for 60 min either alone or in the presence of taurine or ketamine. Ketamine inhibited chemical- or ischemia-induced lipid peroxidation as well as ischemic glutathione depletion. Under the same conditions, taurine failed to affect lipid peroxidation or glutathione. The data show a direct effect of ketamine on lipid peroxidation and point to separate mechanisms of action for ketamine and taurine.

Animals↗
PubMed1990

Metabolic aspects of membrane lipid peroxidation.

Lipid peroxidation is a free radical initiated chain oxidation of unsaturated lipids. With respect to the ubiquity of unsaturated fatty acids in the cellular membranes, the peroxidative damage has the potential to affect many cellular functions. Some of the products of lipid peroxidation are diffusible and can spread the damage far beyond the site of the original free radical attack. There is an interdependency between reactive oxygen species and lipid peroxidation - reactive oxygen species initiate the reactions of lipid peroxidation and are also produced in these reactions as intermediates. The generation of reactive oxygen species can be triggered either by nonenzymatic mechanisms, in which iron ions play the major role, or by a wide range of enzymatic systems. The primary damaging effect of lipid peroxidation is exerted by the interactions with proteins and DNA. These interactions are then revealed at the subcellular (cellular organelles), cellular, and organ levels. The production of lipid peroxides interferes with the regulation of several metabolic pathways. In this review, particular attention is focused on the interaction of non-specifically formed lipid peroxides with the regulatory factors produced by the controlled oxidation of arachidonic acid (prostaglandins and leukotrienes), the effects on ionic pumps and intracellular calcium metabolism, the participation of lipid peroxidation in the ageing process, and the modulation of hormonal regulations by lipid peroxidation. Lipid peroxidation is induced at the level of the whole organism by various extrinsic factors such as ionizing irradiation, physical activity, diet and fasting, and various drugs. There is increasing awareness of the association between pathologic states and lipid peroxidation. Among the most studied are inflammation, ischaemia-reperfusion injury, and atherogenesis. Lipid peroxidation also plays a dual and complex role in cancer. Organisms have developed an efficient multilevel protective system against lipid peroxidation, but this can be overwhelmed by certain pathologies.

Animals↗
PubMed1990

Mechanism of ochratoxin A stimulated lipid peroxidation.

Lipid peroxidation, measured as malondialdehyde formation or by oxygen uptake, was stimulated markedly by the mycotoxin ochratoxin A (OTA) in a reconstituted system consisting of phospholipid vesicles, the flavoprotein NADPH-cytochrome P450 reductase, Fe3+, EDTA and NADPH. Deletion of EDTA lowered the extent of lipid peroxidation but did not eliminate it. Fluorometric and spectrophotometric studies demonstrated the formation of a 1:1 Fe3(+)-OTA complex. The rate of reduction of Fe3+ to Fe2+ was enhanced markedly in the presence of OTA, and there was a further increase in the rate when EDTA was also included. The data indicate that OTA stimulates lipid peroxidation by complexing Fe3+ and facilitating its reduction. Subsequent to oxygen binding, an iron-oxygen complex of undetermined nature initiates lipid peroxidation. Free hydroxyl radicals appear not to participate in lipid peroxidation stimulated by Fe3(+)-OTA.

Animals↗
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↗
PubMed1990

[Protective effect of the antioxidants selenium, vitamin E, and superoxide dismutase on cultured human endothelial cells (ECs) injured by lipid peroxidation].

Lipid peroxidation was induced in cultured human ECs with cumene hydroxide and the protective effect of antioxidants (selenium, vitamin E and SOD) on endothelial cell injury by lipid peroxidation was investigated. The results showed that after administration of antioxidants (Se, Vit E and SOD), concentration of LPO in ECs induced by cumene hydroperoxide was reduced markedly while 6-Keto-PGF1 alpha content in the medium was increased and cell injury was alleviated. These results indicate that through the protective effect on ECs against lipid peroxidation, antioxidants (Se, Vit E and SOD) might play an important role in retarding the process of atherogenesis.

6-Ketoprostaglandin F1 alpha↗
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↗
PubMed1989

Possible generation of hydrogen peroxide and lipid peroxidation of erythrocyte membrane by asbestos: cytotoxic mechanism of asbestos.

We studied a mechanism of hemolysis induced by asbestos particles or silicic acid. This hemolysis was instantly initiated by mixing red blood cells with asbestos particles or silicic acid, and reached a plateau within 10 min. The hemolysis was suppressed by catalase, radical quenchers, deoxygenation, or phospholipids. The degree of the hemolysis was proportional to either the amount of asbestos added into red blood cell suspension or the amount of thiobarbituric acid-reacting substances formed. These findings suggest that in vitro hemolysis induced by asbestos particles (or silicic acid) is ascribed to membrane lipid peroxidation initiated by hydrogen peroxide which was generated by the interaction of the mineral particles with biological membranes.

Asbestos↗
PubMed1989

[The interrelationship of the processes of lipid peroxidation and lipid phospholipase hydrolysis in the synaptosomes].

The influence of Fe2+, alpha-tocopherol, phospholipase A2 and mepacrine on the activity of lipid peroxidation (LPO) and phospholipid hydrolysis (PLH) was studied in synaptosomes. It was established that there is the tight direct interconnection between LPO and PLH in synaptosomes. It is assumed that activation of endogenous phospholipases in neurons is one of the causes of uncompensated LPO-activation during epileptogenesis.

Animals↗
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↗
PubMed1990

Effects of fig latex on lipid peroxidation and CCl4-induced lipid peroxidation in rat liver.

The oral and intraperitoneal effects of fig milk latex on lipid peroxidation and CCl4-induced lipid peroxidation in liver homogenates of female rats were investigated. Oral treatment had no effect, while i.p. administration produced a significant increase in hepatic lipid peroxidation. When the latex was given before CCl4 treatment; it produced no protective effect against CCL4-induced hepatotoxicity. Addition of the latex to the incubation mixture produced a dose-dependent increase in lipid autoxidation, while the chloroform and ether extracts of the latex, as well as heated latex, had no effect on hepatic lipid autoxidation.

Administration, Oral↗