Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PEROXIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed2000

Lipid peroxidation and peroxynitrite in retinal ischemia-reperfusion injury.

PURPOSE: To investigate whether lipid peroxides play a role in retinal cell death due to ischemia-reperfusion injury, whether recombinant human thioredoxin (rhTRX) treatment reduces production of lipid peroxides of the retina, and whether such treatment reduces the number of cells expressing c-Jun and cyclin D1. METHODS: Retinal ischemia was induced in rats by increasing the intraocular pressure to 110 mm Hg for 60 minutes. After reperfusion, immunohistochemical staining for lipid peroxide, peroxynitrite, c-Jun, and cyclin D1 and propidium iodide (PI) staining were performed on retinal sections from animals treated intravenously with and without rhTRX, a free radical scavenger. Quantitative analyses of PI-, c-Jun-, and cyclin D1-positive cells were performed after the ischemic insult. Concentration of lipid peroxides in the retina was determined by the thiobarbituric acid assay. RESULTS: Specific immunostaining for lipid peroxides was seen in the ganglion cell layer at 6 hours after reperfusion, in the inner nuclear layer at 12 hours, and in the outer nuclear layer at 48 hours. Time course studies for PI-positive cells in the three nuclear layers coincided with those of specific immunostaining for lipid peroxides. The specific immunostaining was weakened by pre- and posttreatment with 0.5 mg of rhTRX. The number of PI-, c-Jun-, and cyclin D1-positive cells and the concentration of lipid peroxides were significantly decreased by treatment with rhTRX compared with those of vehicle-treated control rats (P: < 0. 01). CONCLUSIONS: Lipid peroxides formed by free radicals may play a role in neuronal cell death in retinal ischemia-reperfusion injury.

Aldehydes↗
PubMed2006

Effects of different dietary fatty acid supplements upon lipoprotein metabolism and lipid peroxides production in hyperlipidemic rats.

It has been well documented that hypercholesterolemia represents both a common and a dominant, although non-obligatory, risk factor in the progression of atherosclerosis. Research was conducted upon experimentally induced hyperlipidemic animals by means of a custom-tailored atherogenic diet. Cell susceptibility to nonenzyme-induced oxidative stress appears to be influenced by membrane fatty acid composition. This study was undertaken to determine whether differences in lipid peroxidation in steady-state and induced lipid peroxidation is a result of a different fatty acid supplementation. Adult Wistar strain rats of male gender were exposed to an atherogenic diet for a period of 160 days, before randomization into 6 dietary groups with different intragastral oil supplementation. Lipid peroxidation products were measured in 2.5% (w/v) of fresh liver homogenates (Tris-HCl, pH 7.4), by the assay of a thiobarbituric acid reactive substances (TBARS) formation using the procedures described by Okhawa (1979), including modifications (1989) in three different experimental conditions: steady-state (which corresponds to concentration of lipid peroxides in vivo ), spontaneous and metal-stimulated lipid peroxidation. Results were expressed as nmol TBARS per g of liver homogenate, calculated from the absorbency at 532 nm, using TEP as an external standard. This study shows that prolonged atherogenic dietary treatment causes moderate hypercholesterolemia and enhanced hypertriglyceridemia (+34.1% and +114.8, p < 0.001, respectively). Despite the lowering effects of the lipoprotein profiles, resulting from a fatty acid supplementation, at the end of each supplementation period, omega-6 fatty acids (soybean and corn oil) revealed an enhancement in the production of lipid peroxides (TBARS formation) measured in steady-state levels (+22.9%, p < 0.05 and +22.6%, p < 0.05, respectively). When liver homogenates were exposed to Fe2+ and ascorbic acid-induced oxidative stress, lipid peroxidation (LPO) was enhanced in the group treated with soybean oil (omega-6) and fish oil (omega-3; +48.4 %, p < 0.001 and +44.1%, p < 0.001, respectively), but not in the group receiving corn oil. The achieved results support the hypothesis that the process of lipid peroxidation is not always in correlation with the number of double bonds in fatty acids esterified in phospholipid molecules. Consequently, it can be concluded that supplementation of unsaturated fatty acids, in the therapy of cardiovascular diseases, should include the administration of antioxidants, in order to prevent fatty acid decomposition in the case of oxidative insult.

Animals↗
PubMedDate not supplied

[The effect of hemodialysis on lipid peroxidation].

With regard to the variance in the levels of lipid peroxidation products (malonic dialdehyde and diene conjugates) the authors studied the impact of hemodialysis on lipid peroxidation. Transitory activation of lipid peroxidation with a subsequent decrease in the levels of lipid peroxidation products that were lower than initial ones were noted at the initial stages of hemodialysis performed with the use of a DEP-02-02 dialyzer (with a cuprophane membrane). The comparison of the input and output levels of lipid peroxidation products failed to demonstrate any generation of lipid peroxidation products inside the dialyzer. The systemic character of the activation effect in the onset of dialysis was established. It was proved that the effect did not depend on the material used for the membrane as there was no rise in the levels of lipid peroxidation products but a decrease in their concentration when the capillary dialyzers D1 and B2-100 were used. The study of the washings from the cuprophane membrane from the dialyzer DEP-02-02 demonstrated high levels of endotoxin which were several times higher than in those from the same membrane from the dialyzer D2. Endotoxin release into the circulation probably determined the transitory effect of the activation in the onset of the procedure performed with the dialyzer DEP-02-02. The authors discussed the possible origin of high initial levels of lipid peroxidation products observed in patients with terminal chronic renal failure who had undergone hemodialysis.

Adult↗
PubMed1988

Modulation of myoglobin-H2O2-mediated peroxidation reactions by sulfhydryl compounds.

The ability of specific low molecular weight sulfhydryl compounds to inhibit the myoglobin-H2O2 peroxidation of uric acid and arachidonic acid was investigated. alpha-Mercaptopropionyl glycine, N-acetylcysteine, and reduced glutathione inhibited both the oxymyoglobin and metmyoglobin H2O2-mediated peroxidation of uric acid in a dose-dependent manner. The IC50 for each drug ranged between 20 to 100 microM and was dependent on the presence of a reduced sulfhydryl group since neither oxidized glutathione nor methionine effectively blocked uric acid peroxidation. Similar inhibition of oxymyoglobin and metmyoglobin H2O2-mediated peroxidation of arachidonic acid was also observed with alpha-mercaptopropionyl glycine, reduced glutathione, and cysteine. Under conditions of this assay, the ferrous form of myoglobin and H2O2 produced approximately three times the amount of formaldehyde from dimethylsulfoxide than ferric myoglobin (metmyoglobin) and H2O2. However, metmyoglobin and H2O2 were more effective than either oxymyoglobin and deoxymyoglobin in mediating arachidonic acid peroxidation. Further, neither mannitol nor benzoic acid (known scavengers of .OH) effectively blocked myoglobin H2O2-induced peroxidation of either uric acid or arachidonic acid. Visible absorption spectra of oxymyoglobin and metmyoglobin after incubation with H2O2 indicates the formation of a relatively stable ferriperoxide derivative of myoglobin. The formation of the ferriperoxide myoglobin derivative was partially inhibited by the addition of reduced sulfhydryl compounds. These data are consistent with the hypothesis that during reperfusion injury of the ischemic myocardium, the phagocytic cell or intracellular-derived H2O2 may react with myoglobin and initiate peroxidation reactions independent of .OH formation leading to cell injury. The cardioprotective effects of alpha-mercaptopropionyl glycine and other sulfhydryl-containing compounds during reperfusion injury may be attributed, at least in part, to their ability to inhibit myoglobin-H2O2-mediated peroxidation reactions.

Arachidonic Acids↗
PubMed1983

Benzoyl peroxide and epidermal wound healing.

The effectiveness of 10%, 20%, and 50% benzoyl peroxide in a lotion, 20% benzoyl peroxide in a gel, and the effect of the vehicles alone on wound reepithelialization were evaluated in young domestic pigs. Twenty percent benzoyl peroxide suspension in a lotion base substantially increased the rate of reepithelialization by 33% over a seven-day evaluation period. Twenty percent benzoyl peroxide suspension in a gel base and 10% benzoyl peroxide suspension in a lotion base slightly enhanced epidermal resurfacing, while 50% benzoyl peroxide suspension in a lotion base and the vehicle gel retarded healing. Variations in the rate of reepithelialization were observed when different lots of 20% benzoyl peroxide lotions were compared. Chemical analysis of each of the 20% benzoyl peroxide preparations tested disclosed great differences in zinc, magnesium, and sodium content.

Animals↗
PubMed1995

High susceptibility to paraquat-driven lipid peroxidation of cultured hepatocytes loaded with linolenic acid.

Rat hepatocytes cultured without (normal cells) and with 1 mM alpha-linolenic acid-bovine serum albumin complex (alpha-linolenic acid [LNA]-loaded cells) for 12 hr were challenged with paraquat at concentrations ranging from 0.01 to 5 mM. The addition of paraquat to normal hepatocytes induced a relatively low level of lipid peroxidation as measured by the accumulation of malondialdehyde in the medium, even at a high paraquat concentration that caused severe cell injury. LNA-loaded hepatocytes markedly underwent lipid peroxidation on addition of paraquat, with a rise in the malondialdehyde accumulation beginning at the lowest concentration used (0.01 mM). The enhanced lipid peroxidation induced in LNA-loaded hepatocytes by the addition of paraquat was accompanied by the occurrence of cell injury at noncytotoxic paraquat concentrations for normal cells. Of further importance was that in LNA-loaded cells, lipid peroxidation promptly occurred after the addition of paraquat and was followed by the loss of cell viability. Addition of antioxidants such as N,N'-diphenyl-p-phenylenediamine and alpha-tocopherol with paraquat prevented lipid peroxidation in both normal and LNA-loaded hepatocytes but protected only the latter cells from cell injury. Neither lipid peroxidation nor cell injury in either group of hepatocytes was prevented by the presence of .OH scavengers such as mannitol and dimethyl sulfoxide. In addition, paraquat-driven lipid peroxidation in LNA-loaded hepatocytes was promoted by the addition of ascorbate but was rather suppressed by the addition of H2O2. In conclusion, it is likely that the addition of paraquat induced Fe(++)-lipid hydroperoxide-dependent lipid peroxidation that led to lethal cell injury in LNA-loaded hepatocytes.

Animals↗
PubMed1997

A new model for the pathophysiology of Alzheimer's disease. Aluminium toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin.

OBJECTIVES: Although Alzheimer's disease (AD) is the leading cause of dementia in developed countries, there is an as yet unexplained lower prevalence of the disease in parts of Africa. AD is characterised by a catastrophic loss of neurons; free radicals (oxidative toxins) have been implicated in the destruction of the cells through the process of lipid peroxidative damage of cell membranes. Previously aluminium (Al) and a fragment of beta amyloid (A beta 25-35) were shown to exacerbate free-radical damage, while melatonin reduced this effect. The aim of the present study was: (i) to investigate the conditions determining the toxicity of Al and A beta 25-35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD. DESIGN: An in vitro model system was used in which free radicals were generated, causing lipid peroxidation of platelet membranes, thus simulating the disease process found in the brain. RESULTS: 1. Al and A beta 25-35 caused lipid peroxidation in the presence of the iron (II) ion (Pe2+), Al being more toxic than A beta 25-35. 2. A beta 25-35 attenuated the lipid peroxidation promoted by Al. 3. Hydrogen peroxide (H2O2) greatly exacerbated the toxicity of Al and A beta 25-35. 4. Melatonin prevented lipid peroxidation by Al and A beta 25-35 in the absence of H2O2, but only reduced the process when H2O2 was present. CONCLUSIONS: In the light of the results obtained from the present study, the following hypotheses are formulated. 1. In AD, excessive quantities of Al are taken up into the brain, where the Al exacerbates iron-induced lipid peroxidation in the lysosomes. 2. In response, the normal synthetic pathway of amyloid protein is altered to produce A beta fragments which attenuate the toxicity of Al. In the process of sequestering the Al and iron, immature plaques are formed in the brain. 3. Microglia are activated, in an attempt to destroy the plaques by secreting reactive oxygen species such as H2O2. At this point in the disease process, lipid peroxidation causes a catastrophic loss of brain cells. 4. Melatonin, together with other free radical scavengers in the brain, reduces the free-radical damage caused by Al and A beta, except in the latter stages of the disease process. Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why AD is more prevalent in these countries than in rural Africa.

Aluminum↗
PubMed2000

Characterization of peroxide ions in hydroxyapatite lattice.

The incorporation of peroxide ions was confirmed in the heat treatment of hydroxyapatite (HA) powder under air as well as under oxygen atmosphere, by using X-ray diffraction, Raman, and infrared spectroscopy. Peroxide ions associated with vacancies were sited in the channel of HA lattice along the c-axis through the substitution of a portion of OH radicals. The molecular ions constituted a symmetric vibrator with a stretching vibration active in Raman spectrometry. This vibration was recorded at 750 cm(-1) in the Raman spectra of O(2)(2-)-containing HA samples. The final product was a solid solution of hydroxyl- and peroxide-apatite. However, the existence of peroxide ions in the HA lattice caused the contraction of the unit-cell dimensions of HA materials. In addition, a new hydrogen bond was formed between peroxide ions and adjacent OH radicals by using molecular spectroscopy analysis. During annealing treatment in air, peroxide ions decomposed and the substituted OH radicals re-enter the HA lattice, resulting in the elimination of the structural aberrations caused by the incorporation of peroxide ions. Concentration of the peroxide ions included in HA samples was measured by chemical analysis.

Biocompatible Materials↗
PubMed1993

Analysis of lipid peroxidation mechanisms in human spermatozoa.

The mechanisms by which ferrous ion promoters induce malondialdehyde generation by human spermatozoa have been investigated in order to provide a rational basis for the quantification and interpretation of lipid peroxidation assays. Incubation of human spermatozoa with a ferrous ion promoter in the presence of thiobarbituric acid (TBA) led to the generation of the bone fide malondialdehyde-TBA adduct. The importance of iron in the stimulation of lipid peroxidation was emphasized by the ability of Desferal and EDTA to suppress malondialdehyde generation. Paradoxically, when the concentration of EDTA relative to iron was equimolar or greater, the suppression of malondialdehyde formation was accompanied by the generation of hydroxyl radicals. These results suggested that the addition of promoter did not effect the first-chain initiation of lipid peroxidation but favored an alternative mechanism involving the catalytic decomposition of pre-existing lipid peroxides. This conclusion was reinforced by the inability of reagents that would limit the formation (superoxide dismutase and/or catalase) or availability (mannitol, formate) of hydroxyl radicals, to influence malondialdehyde generation. While hydroxyl radicals were not directly involved in Fe(2+)-promoted malondialdehyde generation, the existence of significant correlations between reactive oxygen species production and the outcome of the TBA assay, suggested that Fenton chemistry might be important in the initiation of peroxidative damage. It is proposed that the impeded propagation of peroxidation initiated by Fenton or Haber Weiss reactions would lead to the accumulation of lipid peroxides in the spermatozoa and it is these peroxides that are induced to decompose during the Fe(2+)-promoted TBA assay, stimulating a lipoperoxidative chain reaction and malondialdehyde formation.

Deferoxamine↗
PubMed2005

Lipid peroxide formation in relation to membrane stability of fresh and frozen thawed stallion spermatozoa.

In this study we used a new method to detect reactive oxygen species (ROS) induced damage at the level of the sperm plasma membrane in fresh and frozen-thawed stallion sperm. Lipid peroxidation (LPO) in sperm cells was assessed by a fluorescent assay involving the labeling of stallion sperm with the LPO reporter probe C11-BODIPY(581/591). The peroxidation dependent spectral emission shift of this membrane probe could be localized using inverted spectral confocal microscopy and quantified on living and deteriorated sperm cells using flow cytometry. Mass spectrometric analysis of the main endogenous lipid class, phosphatidylcholine (PC), was carried out to determine the formation of hydroxy- and hydroperoxyphosphatidylcholine in fresh sperm cells. Peroxidation as reported by the fluorescent probe corresponded with the presence of hydroxy- and hydroperoxyphosphatidylcholine in the sperm membranes, which are early stage products of LPO. This allowed us to correlate endogenous LPO with localization of this process in the living sperm cells. In absence of peroxidation inducers, only relatively little peroxidation was noted in fresh sperm cells whereas some mid-piece specific probe oxidation was noted for frozen-thawed sperm cells. After induction of peroxidation in fresh and frozen-thawed sperm cells with the 0.1 mM of lipid soluble ROS tert-butylhydrogen peroxide (t-BUT) intense probe oxidation was produced in the mid-piece, whereas the probe remained intact in the sperm head, demonstrating antioxidant activity in the head of fresh sperm cells. At higher levels of t-BUT, probe peroxidation was also noted for the sperm head followed by a loss of membranes there. Frozen-thawed sperm were more vulnerable to t-BUT than fresh sperm. The potential importance of the new assays for sperm assessments is discussed.

Animals↗
PubMed1995

Hemoglobin-induced lipid peroxidation in the retina: a possible mechanism for macular degeneration.

To investigate a possible link between subretinal hemorrhage and macular degeneration, oxyhemoglobin (HbO2) or methemoglobin (metHb) was incubated with retinal homogenate and unsaturated phospholipid peroxidation was monitored by (a) assay of thiobarbituric acid-reactive substances (TBARS), (b) luminescence originating from an energy transfer of lipid-degraded products to rose bengal, and (c) the decrease in composition of highly unsaturated fatty acids of phospholipids. TBARS formation and rose bengal luminescence in the case of metHb-induced lipid peroxidation were about 1.5 times greater than those in HbO2-induced lipid peroxidation. alpha-Tocopherol, a lipid-soluble antioxidant, and docosahexaenoic acid, a major unsaturated fatty acid, were slightly more rapidly decomposed after a 60-min incubation with metHb than with HbO2 at the same concentration. Atomic absorption analysis revealed that an equal concentration of iron was released from both HbO2 and metHb during incubation with retinal homogenates. The released iron may promote microsomal phospholipid peroxidation in the presence of endogenous ascorbate or NADPH-dependent cytochrome P-450 reductase because ascorbate oxidase and p-chloromercuribenzoic acid (an inhibitor of sulfhydryl enzymes) inhibited metHb- or HbO2-induced lipid peroxidation. MetHb-induced lipid peroxidation in retina was inhibited by KCN or NaN3, which binds to FeIII of metHb. KCN or NaN3 had no effect on HbO2-induced lipid peroxidation, because conversion of HbO2 to metHb, which can proceed in HbO2 incubated with phospholipid liposome, did not occur in retinal homogenates. It is concluded that metHb induces peroxidation of retinal unsaturated phospholipids (1) directly and (2) by releasing iron.

Animals↗
PubMed1996

Ferritin stimulation of lipid peroxidation by microsomes after chronic ethanol treatment: role of cytochrome P4502E1.

Ferritin is the major storage form of iron within cells, and iron released from ferritin has been shown to stimulate lipid peroxidation. Microsomes from rats chronically fed ethanol are more active in generating reactive oxygen intermediates than control microsomes. Since superoxide is one of the reductants capable of releasing iron from ferritin, and superoxide generation by microsomes is increased after chronic ethanol treatment, the ability of ferritin to stimulate lipid peroxidation of microsomes isolated from control rats and rats treated chronically with ethanol was evaluated. Ferritin was much more effective in stimulating lipid peroxidation of microsomes after ethanol treatment; net increases in thiobarbituric acid-reactive components by ferritin were 4-fold greater in the presence of NADPH with microsomes from the ethanol-treated rats compared to pair-fed controls and 10-fold greater with NADH as the microsomal reductant. Net increases in chemiluminescence by ferritin were about 10-fold greater with microsomes from the ethanol-treated rats. The NADPH- and NADH-dependent increases in lipid peroxidation produced by ferritin were prevented by superoxide dismutase, which lowered the rates found in the presence of ferritin to values found in the absence of ferritin. Catalase and hydroxyl radical scavengers had no effect on the stimulation by ferritin. Nonheme iron chelators prevented the ferritin stimulation as did glutathione, propylgallate, and trolox. Basal rates of lipid peroxidation were inhibited by anti-CYP2E1 IgG; the stimulation by ferritin was decreased by anti-CYP2E1 IgG. These results show that microsomes from ethanol-fed rats are more reactive than control microsomes in interacting with ferritin to produce oxidants capable of catalyzing lipid peroxidation. The inhibition of the ferritin-catalyzed lipid peroxidation by superoxide dismutase and anti-CYP2E1 IgG is consistent with a role for CYP2E1-generated superoxide radical in mobilizing iron from ferritin and in the subsequent catalysis of lipid peroxidation. Since ferritin is the major cellular storage form of iron, increased mobilization of iron from ferritin by CYP2E1-derived superoxide radical may play a role in the development of oxidative stress after ethanol treatment.

Alcoholism↗
PubMed1999

Nitric oxide inhibits iron-induced lipid peroxidation in HL-60 cells.

Nitric oxide ((*)NO) can protect cells against the detrimental effects of reactive oxygen species. Using low-density lipoprotein as well as model systems, it has been demonstrated that (*)NO can serve as a chain-breaking antioxidant to blunt lipid peroxidation. To test the hypothesis that (*)NO can serve as a chain-breaking antioxidant in cell membranes, we examined the effect of (*)NO on iron-induced lipid peroxidation in human leukemia cells. We exposed HL-60 cells to an oxidative stress (20 microM Fe(2+)) and monitored the consumption of oxygen as a measure of lipid peroxidation. Oxygen consumption was arrested by the addition of (*)NO as a saturated aqueous solution. The duration of inhibition of oxygen consumption by (*)NO was concentration-dependent in the 0.4-1.8 microM range. The inhibition ended upon depletion of (*)NO. The addition of (*)NO prior to initiation of peroxidation delayed the onset of peroxidation; the nearer in time it was before Fe(2+) addition, the longer the inhibition. Depletion of cellular glutathione levels by d, l-buthionine-S,R-sulfoximine prior to Fe(2+) addition resulted in a more rapid initial rate of oxygen depletion and a shorter time for the (*)NO-induced inhibition of oxygen consumption. Complementary studies of this iron-induced lipid peroxidation, using thiobarbituric acid reactive substances as a marker, also demonstrated the protective effects of (*)NO. This protection of cells against lipid peroxidation also manifested itself as a reduction in trypan blue uptake, an observation demonstrating the protective effects of (*)NO on membrane integrity. We conclude that (*)NO protects HL-60 human leukemia cells from lipid peroxidation and that this protection ameliorates the toxicity of the oxidation processes initiated by Fe(2+) and dioxygen.

Cell Membrane↗
PubMed1994

Phospholipid peroxidation after 60 min of global ischaemia and 10 min of reperfusion. A study in the isolated rat heart.

Peroxidation of polyunsaturated fatty acids in cell membranes is thought to be a crucial factor in the cascade leading to reperfusion damage in the myocardium. However, some studies also describe increased lipid peroxidation in ischaemic tissue. The present study therefore examines phospholipid peroxidation after 60 min of global ischaemia and during the initial phase of reperfusion in isolated Langendorff-perfused rat hearts. Lipids were extracted from these hearts and separated into phospholipid, triglyceride and non-esterified fatty acid fractions. The phospholipid fraction was hydrolysed with phospholipase A2, and reverse-phase high performance liquid chromatography of the fatty acids derived from the phospholipids was performed. Peroxidized polyunsaturated fatty acids were separated from unchanged fatty acids and amounts of monohydroxy or monohydroperoxy isomers were quantified by measuring conjugated dienes by UV absorption (235 nm). Phospholipids from ischaemic as well as free-radical-exposed tissue contained increased levels of peroxidized polyunsaturated fatty acids (20.7 +/- 2.4 and 20.5 +/- 2.3 respectively, v 11.8 +/- 1.4 units/mg dry weight in controls). After 2-10 min of reperfusion, a significant increase in phospholipid peroxidation was no longer detected (12.5 +/- 1.2 units/mg). The amount and the composition of non-esterified fatty acids were examined by gas chromatography. Ischaemia significantly increased both the amount of non-esterified fatty acids (1.5 +/- 0.8 v 4.9 +/- 1.8 nmol/mg dry wt) as well as the percentage composed of arachidonic acid (3.4 +/- 3.2% v 7.4 +/- 1.4%). Fatty acid levels remained elevated during reperfusion (5.5 +/- 1.9 nmol/mg and 7.0 +/- 1.4%). In conclusion, our results have demonstrated that prolonged ischaemia alone caused phospholipid peroxidation as well as accumulation of non-esterified arachidonic acid. There was no sign of further phospholipid peroxidation during reperfusion.

Animals↗
PubMed1991

The possible role of phospholipase A2 in hepatic microsomal lipid peroxidation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats.

The induction of lipid peroxidation in hepatic microsomes of rodents treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is well documented. The potential mechanisms involved in TCDD-induced microsomal lipid peroxidation were investigated, using selected inhibitors and free radical scavengers in vitro. Rats were treated with 40 micrograms TCDD/kg orally as a single dose. Inhibitors of phospholipase A2, including a variety of phenothiazines, dibucaine, imipramine, and verapamil, inhibited in vitro microsomal lipid peroxidation in response to TCDD administration. In addition, the lipoxygenase inhibitor quercetin, and the hydrogen peroxide scavenger aminopyrine inhibited lipid peroxidation with microsomes from TCDD-treated rats. The singlet oxygen scavenger beta-carotene, the cytochrome P-450 substrate benzphetamine, and the cyclooxygenase inhibitor indomethacin produced moderate enhancement of hepatic microsomal lipid peroxidation. The results suggest that activation of phospholipase A2 may play a critical role in the metabolic events associated with hepatotoxicity and ultimate cell death produced by TCDD. The results also support the involvement of hydrogen peroxide in TCDD-induced microsomal lipid peroxidation.

Aminopyrine↗
PubMed1980

Relative susceptibility of microsomes from lung, heart, liver, kidney, brain and testes to lipid peroxidation: correlation with vitamin E content.

Rates of in vitro lipid peroxidation of microsomes and homogenates were found to vary widely among different tissues and species. In rats and rabbits, lung microsomes peroxidized at a 25- to 50-fold lower rate than liver, kidney, testes and brain microsomes. Heart microsomes peroxidized at a rate slightly greater than, but most similar to, lung microsomes. Comparison of tissue homogenates also revealed the unique resistance of lung and heart to lipid peroxidation. The ratio of vitamin E to peroxidizable polyunsaturated fatty acids in lung and heart microsomes was several-fold higher than in microsomes from the other tissues studied, which accounted for the relative resistance of lung and heart to lipid peroxidation. Liposomes of extracted rat lung microsomal lipid were also resistant to peroxidation and the amount of vitamin E contained in the lung lipid extract was sufficient to confer the same degree of resistance when incorporated into an equivalent amount of rat liver lipid. Higher rates of peroxidation in mouse lung microsomes relative to rabbit, rat and human lung microsomes were similarly correlated with a lower ratio of vitamin E to peroxidizable fatty acids in mouse lung microsomes. These data provide strong support for the role of vitamin E as the major cellular antioxidant, especially in the highly oxygenated tissues of heart and lung, and demonstrate the utility of the microsomal system in characterizing tissue differences in susceptibility to peroxidative membrane decomposition.

Animals↗
PubMedDate not supplied

Does lead provoke the peroxidation process in rat brain synaptosomes?

Up to now there has been no information concerning the effect of lead on the peroxidation process in brain nerve endings. We have examined whether lead acetate (in chronic and acute models of toxicity in vivo and in vitro) affected the level of free radicals in synaptosomes obtained from rat brain. Simultaneously, we have checked the effect of peroxidation of Pb2+ on brain homogenates and microsomal fraction. Our results indicated that the lead level in synaptosomal fraction obtained from lead-treated rats was much higher than in controls. We did not observe induction of spontaneous and Fe(3+)-dependent peroxidation either in synaptosomes or in homogenates and brain microsomes after chronic and acute lead administration to the rats. Lead itself also did not enhance both processes when added in vitro to the control brain synaptosomes in micromolar concentrations. The lack of the lead effect on the peroxidation process in subcellular fractions of brain was rather surprising, because lead is known to be the accelerator of Fe(3+)-dependent peroxidation processes in liver. Additionally, livers from rats under the same toxicity conditions were examined. We have found that lead did not provoke spontaneous peroxidation in liver, but contrary to brain fractions, it drastically increased iron-dependent peroxidation in liver homogenates and microsomes. The lack of the effect of lead on inducing peroxidation processes in brain is probably the consequence of the brain having stronger protective mechanisms against its toxicity than the liver.

Acute Disease↗
PubMed1998

Ascorbate-stimulated lipid peroxidation and non-heme iron concentrations in Alzheimer disease.

Lipid peroxidation has been suggested to be a potential cause of neuronal damage in neurodegenerative diseases. Changes in several parameters of lipid peroxidation, including basal (unstimulated) lipid peroxidation, stimulated lipid peroxidation, tissue iron concentrations, and the concentrations of some oxygen radical scavengers, have been reported in neurodegenerative diseases. However, the in vitro interaction of oxygen radical scavengers and stimulated lipid peroxidation in neurodegenerative disease has been less well-studied. The purpose of the present study was to determine the effects of oxygen radical scavengers on ascorbate-stimulated lipid peroxidation in Alzheimer disease (AD). We have found that some parameters of ascorbate-stimulated lipid peroxidation are altered in AD and that the effects of superoxide dismutase (SOD) on ascorbate-stimulated lipid peroxidation are significantly different in AD as compared to aged.

Aged↗