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PubMed2004

Moderate intensity resistance exercise, plus or minus soy intake: effects on serum lipid peroxides in young adult males.

Lipid peroxides can be both a product and an initiator of oxidant stress. Conceivably, exercise can either increase concentrations of lipid peroxides (by causing oxidant stress), or decrease them (by accelerating peroxide breakdown). The net effect could depend on exercise intensity and nutritional intake of antioxidants. The present study examined the response of serum lipid peroxides to the combination of moderate intensity, weight resistance exercise plus intake of soy protein, a source of antioxidant phytochemicals. Recreationally trained, young adult men (N = 18) consumed soy protein or antioxidant-poor whey protein for 4 weeks (40 g protein/d) before a session of moderate intensity, weight resistance exercise. In the soy group, exercise decreased values for serum lipid peroxides at 5 min, 3 h, and 24 h post-exercise. The whey group showed the depression only at 24 h. In both the soy and whey groups, a small rise was seen for interleukin-8, which is consistent with the idea that the exercise session induced a moderate muscle stress. In summary, a moderate intensity, weight resistance exercise session, despite inducing mild inflammation, depressed plasma serum peroxide values, especially when combined with 4 weeks of soy consumption.

Adolescent↗

PubMed2000

Urea hydrogen peroxide reduces the numbers of lactobacilli, nourishes yeast, and leaves no residues in the ethanol fermentation.

Urea hydrogen peroxide (UHP) at a concentration of 30 to 32 mmol/liter reduced the numbers of five Lactobacillus spp. (Lactobacillus plantarum, L. paracasei, Lactobacillus sp. strain 3, L. rhamnosus, and L. fermentum) from approximately 10(7) to approximately 10(2) CFU/ml in a 2-h preincubation at 30 degrees C of normal-gravity wheat mash at approximately 21 g of dissolved solids per ml containing normal levels of suspended grain particles. Fermentation was completed 36 h after inoculation of Saccharomyces cerevisiae in the presence of UHP, even when wheat mash was deliberately contaminated (infected) with L. paracasei at approximately 10(7) CFU/ml. There were no significant differences in the maximum ethanol produced between treatments when urea hydrogen peroxide was used to kill the bacteria and controls (in which no bacteria were added). However, the presence of L. paracasei at approximately 10(7) CFU/ml without added agent resulted in a 5.84% reduction in the maximum ethanol produced compared to the control. The bactericidal activity of UHP is greatly affected by the presence of particulate matter. In fact, only 2 mmol of urea hydrogen peroxide per liter was required for disinfection when mashes had little or no particulate matter present. No significant differences were observed in the decomposition of hydrogen peroxide in normal-gravity wheat mash at 30 degrees C whether the bactericidal agent was added as H(2)O(2) or as urea hydrogen peroxide. NADH peroxidase activity (involved in degrading H(2)O(2)) increased significantly (P = 0.05) in the presence of 0.75 mM hydrogen peroxide (sublethal level) in all five strains of lactobacilli tested but did not persist in cells regrown in the absence of H(2)O(2). H(2)O(2)-resistant mutants were not expected or found when lethal levels of H(2)O(2) or UHP were used. Contaminating lactobacilli can be effectively managed by UHP, a compound which when used at ca. 30 mmol/liter happens to provide near-optimum levels of assimilable nitrogen and oxygen that aid in vigorous fermentation performance by yeast.

Carbamide Peroxide↗

PubMed1991

Simple and specific test for measuring lipid peroxides in plasma.

The specificity of an iodometric assay for measuring lipid peroxides in lipoproteins was tested, compared with the fluorimetric thiobarbituric acid assay, and adopted for detecting lipid peroxide in plasma samples. Oxidation of low density lipoproteins in vitro by Cu2+, lipoxidase, and phagocytosing polymorphonuclear leucocytes was sensitively detected by the iodometric assay. Unlike the thiobarbituric acid assay, neither non-lipid substances commonly present in plasma, nor platelet or polymorphonuclear leucocyte by-products interfered with the iodometric assay. The iodometric assay measured a normal mean (SD) plasma lipid peroxide concentration of 10.8 (2.1) microM; n = 63. Two weeks after the start of a high cholesterol diet in rabbits (n = 5), a sixfold increase in plasma lipid peroxide concentrations was measured by iodometric assay. The specificity of a simple and sensitive iodometric test of lipid peroxidation was superior to that of the thiobarbituric acid assay. This iodometric assay should therefore provide a much more accurate assessment of lipid peroxide in plasma samples.

Adult↗

PubMed1996

No direct evidence of increased lipid peroxidation in hemodialysis patients.

Lipid peroxidation, as measured by the thiobarbituric acid test, has been reported to have increased in hemodialysis (HD) patients, even though the test has low specificity in vivo. Conjugated diene fatty acid (CDFA) hydroperoxides are formed during lipid peroxidation, but not all conjugated dienes (CD) detected in humans originate from lipid peroxidation: octadeca-9,11-dienoic acid, a nonhydroperoxide CD derivative of linoleic acid (CDLA), has a dietary origin. We evaluated CDFA hydroperoxides, CDLA and linoleic acid, using high-performance liquid chromatography, in lipids extracted from plasma, adipose tissue and RBC membranes obtained from 25 patients treated with HD, 16 patients treated with hemodiafiltration (HDF) and 29 controls. No differences in the levels of CDFA hydroperoxides and linoleic acid were seen in any of the groups. Concentrations of CDLA were found to be significantly high in the adipose tissue and low in the RBC membranes of HD patients. HDF-treated patients showed the same results as HD patients. No direct evidence of increased lipid peroxidation was found in HD patients. This does not exclude the possibility that lipid peroxidation is increased and escapes direct detection due to the body's homeostatic control eliminating the increased production of hydroperoxides. Both HD- and HDF-treated patients showed a significant change in CDLA concentrations, either in the adipose tissue, or in the RBC membranes. These dietary CD may be mistaken for markers of lipid peroxidation by conventional methodologies.

Adipose Tissue↗

PubMed1996

Increased lipid peroxidation by rat liver microsomes in experimental renal failure.

This study investigated the peroxidative state of renal failure by measuring lipid peroxidation. The generation of lipid peroxides by rat hepatic microsomes was compared between experimental renal failure caused by 7/8 nephrectomy and healthy control animals. The concentrations of BUN at the point of sacrifice were 84.2 +/- 18.4 (mean +/- SD) in nephrectomized and 19.8 +/- 4.3 mg/dl in the control group (p < 0.01, n = 5). Microsomal generation of thiobarbituric acid reactive substance was 31.2 +/- 2.8 in the nephrectomized group and 20.9 +/- 4.9 nmol/incubation/min in the control group. There was a significant difference between the groups (p < 0.01, n = 5). In summary, the generation rate of lipid peroxides in the microsomes obtained from the rats with experimental renal failure was significantly higher than the control. This study confirms an increased peroxidative state, and specifies one of the sites of increased lipid peroxide generation in renal failure.

Animals↗

PubMed1990

A 21-aminosteroid reduces hydrogen peroxide generation by and chemiluminescence of stimulated human leukocytes.

Leukocytes recruited to regions of focal cerebral ischemia may contribute to tissue injury by their ability to promote inflammation. A novel group of drugs, the 21-aminosteroids, have been observed to reduce neurologic damage and vasogenic cerebral edema in animal models of stroke by inhibiting lipid peroxidation. Production of hydrogen peroxide and free radicals by leukocytes during the inflammatory response may contribute to lipid peroxidation and other consequences of free radical-mediated tissue injury. We assessed the effect of U74500A, a 21-aminosteroid, on the generation of hydrogen peroxide by and on the chemiluminescence of stimulated polymorphonuclear leukocytes and monocytes from normal humans. U74500A significantly reduced the generation of hydrogen peroxide by polymorphonuclear leukocytes (p less than 0.001) and monocytes (p less than 0.01) in a dose-dependent manner. Monocyte chemiluminescence was also significantly inhibited (p less than 0.05), but polymorphonuclear leukocyte-associated chemiluminescence was unchanged. Our results indicate that U74500A can reduce the concentration of oxygen metabolites associated with stimulated human leukocytes, and this effect may explain in part how 21-aminosteroids reduce lipid peroxidation, ischemic injury, and vasogenic edema.

Adult↗

PubMed2000

Plasma and erythrocyte lipid peroxidation levels in patients with testis tumor after orchiectomy.

Plasma and erythrocyte lipid peroxidation levels of 20 patients with histopathologically confirmed testis cancer and 20 healthy control individuals were studied between November 1995 and June 1997. The group with testis cancer had a mean age of 24.8+/-8.2 yr and the control group's mean age was 28.3+/-6.9 yr. Stage distribution of the testis cancer cases were 4 of stage A, 10 of stage B, and 6 of stage C. Blood samples of the patients were drawn after orchiectomy and after 12 h fasting before chemotherapy. Mean plasma and erythrocyte lipid peroxidation levels were detected to be 14.51+/-5.30 nmol malondialdehide (MDA)/mL and 9.30+/-2.06 nmol MDA/g hemoglobin (Hb), respectively, in the testis cancer group, whereas the healthy control group had mean plasma and erythrocyte lipid peroxidation levels of 10.7+/-1.82 nmol MDA/mL and 6.18+/-1.68 nmol MDA/g Hb, respectively. Plasma and erythrocyte lipid peroxidation values of the testis cancer patients were determined to be statistically significantly higher than that of the health control group (p < 0.001, p < 0.001). No significant correlation was determined between plasma, erythrocyte lipid peroxidation levels and tumor markers. In conclusion, it can be said that an increase in the lipid peroxidation may play a role in the pathogenesis of testis carcinomas in addition to the other causes.

Adult↗

PubMed1993

Inhibition of the iron-catalysed formation of hydroxyl radicals by nitrosouracil derivatives: protection of mitochondrial membranes against lipid peroxidation.

A new series of metal ligands containing the 1,3-dimethyl-6-amino-5- nitrosouracil moiety has been synthesized and they have been studied as potential inhibitors of iron-dependent lipid peroxidation. For this purpose, these new derivatives have been tested in the Fenton induced deoxyribose degradation assay, which allows a quantitative measurement of their inhibitory effect towards hydroxyl radical generation. When iron(II) is complexed by these ligands, a strong inhibition of deoxyribose degradation is observed, especially in the case of tris-[2-(1,3-dimethyl-5-nitrosouracil-6-yl)aminoethyl] amine (5). This inhibitory effect is clearly related to a specific complexation of iron(II) and is not due to the direct scavenging of hydroxyl radical by the ligand. Inhibition of the iron mediated Fenton reaction presumably results from inactivation of the reactivity of the metal center towards hydrogen peroxide. These derivatives, as well as long alkyl chain substituted nitrosouracils were evaluated in the protection of biological membranes against lipid peroxidation (induced by iron(II)/dihydroxyfumaric acid and determined with the 2-thiobarbituric acid test). Ligand 5 inhibited lipid peroxidation at a rate similar to Desferal (desferrioxamine B) and slightly higher than bathophenanthroline sulphonate (BPS), which are respectively good iron(III) and iron(II) chelators. When covalently bound with a long alkyl chain, the increase of lipophilic character of the ligand allows its location near the mitochondrial membrane, where lipid peroxidation occurs. Lower concentrations (IC50 = 4 microM) are then necessary to inhibit lipid peroxidation. This IC50 concentration should be compared to those obtained for Trolox (IC50 = 3 microM) or the 21-aminosteroid U74500A (IC50 = 1 microM) described previously.

Animals↗

PubMed1998

alpha-tocopherol protects the peroxidative modification of LDL to be recognized by LDL receptors.

BACKGROUND: Peroxidatively modified low-density lipoprotein (LDL) may contribute to the atherosclerotic process; therefore, protecting LDL against peroxidation may reduce or retard the progression of atherosclerosis. We evaluated the effect of alpha-tocopherol on copper-catalyzed LDL peroxidative modification. METHODS: The protective effects of alpha-tocopherol on copper-catalyzed LDL peroxidative modification were examined by measurement of the concentration of lipid hydroperoxides in LDL and by the provision of LDL cholesterol to lymphocytes via the LDL receptor-mediated pathway. RESULTS: The measurement of concentration of lipid hydroperoxides in LDL showed that alpha-tocopherol inhibited the peroxidative modification of LDL. Also, alpha-tocopherol preserved the ability of LDL to be recognized by LDL receptors in peripheral blood lymphocytes to the same extent as native LDL. CONCLUSION: These findings indicate that alpha-tocopherol may protect LDL against peroxidative modification, maintaining its ability to act as a ligand for LDL receptors in vivo.

Adult↗

PubMed2001

Ascorbic acid protects against peroxidative modification of low-density lipoprotein, maintaining its recognition by LDL receptors.

Peroxidatively modified low-density lipoprotein (LDL) may contribute to atherosclerotic processes; therefore, protecting LDL against peroxidation may thus reduce or retard the progression of atherosclerosis. We have evaluated the protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification. The protective effects of ascorbic acid on copper-catalyzed LDL peroxidative modification were examined by measurement of concentration of lipid hydroperoxides in LDL and by the provision of LDL cholesterol to lymphocytes via LDL receptor-mediated pathway. The measurement of concentration of lipid hydroperoxides in LDL showed that ascorbic acid inhibited peroxidative modification of LDL. Also, ascorbic acid preserved the ability of LDL to be recognized by LDL receptors in peripheral blood lymphocytes to the same extent as native LDL. These findings indicate that ascorbic acid may protect LDL against peroxidative modification, maintaining its ability to act as a ligand for LDL receptors in vivo.

Adult↗

PubMed1999

Secondary radicals derived from chloramines of apolipoprotein B-100 contribute to HOCl-induced lipid peroxidation of low-density lipoproteins.

Oxidation of low-density lipoproteins (LDL) is thought to contribute to atherogenesis. Although there is increasing evidence for a role of myeloperoxidase-derived oxidants such as hypochlorite (HOCl), the mechanism by which HOCl modifies LDL remains controversial. Some studies report the protein component to be the major site of attack, whereas others describe extensive lipid peroxidation. The present study addresses this controversy. The results obtained are consistent with the hypothesis that radical-induced oxidation of LDL's lipids by HOCl is a secondary reaction, with most HOCl consumed via rapid, non-radical reaction with apolipoprotein B-100. Subsequent incubation of HOCl-treated LDL gives rise to lipid peroxidation and antioxidant consumption in a time-dependent manner. Similarly, with myeloperoxidase/H2O2/Cl- (the source of HOCl in vivo), protein oxidation is rapid and followed by an extended period of lipid peroxidation during which further protein oxidation does not occur. The secondary lipid peroxidation process involves EPR-detectable radicals, is attenuated by a radical trap or treatment of HOCl-oxidized LDL with methionine, and occurs less rapidly when the lipoprotein was depleted of alpha-tocopherol. The initial reaction of low concentrations of HOCl (400-fold or 800-fold molar excess) with LDL therefore seems to occur primarily by two-electron reactions with side-chain sites on apolipoprotein B-100. Some of the initial reaction products, identified as lysine-residue-derived chloramines, subsequently undergo homolytic (one-electron) reactions to give radicals that initiate antioxidant consumption and lipid oxidation via tocopherol-mediated peroxidation. The identification of these chloramines, and the radicals derived from them, as initiating agents in LDL lipid peroxidation offers potential new targets for antioxidative therapy in atherogenesis.

Apolipoprotein B-100↗

PubMed2000

HPLC analysis of lipid-derived polyunsaturated fatty acid peroxidation products in oxidatively modified human plasma.

BACKGROUND: Lipid peroxidation is a prominent manifestation of free radical activity and oxidative stress in biological systems. Diverse methodologies have been developed that measure a variety of lipid peroxidation products used as markers of lipid peroxidation processes. METHODS: Hydroxy and hydroperoxy polyunsaturated fatty acid (PUFA) peroxidation products were analyzed in human blood plasma by reversed-phase HPLC after liquid-liquid extraction of total lipids and alkaline hydrolysis of lipid esters to liberate free PUFAs. An isocratic mobile phase containing 1 g/L acetic acid-acetonitrile-tetrahydrofuran (52:30:18, by volume) over 60 min duration, with ultraviolet absorbance detection at 236 nm by photodiode array, enabled the resolution and quantification of 13 regioisomeric hydroxy and hydroperoxy PUFAs. RESULTS: As little as 250 microL of human plasma was utilized with an analytical range of 0.033-1.6 micromol/L for each compound. Intra- and interassay CVs for all compounds detected in normal or oxidatively modified human plasma were 3.2-11% and 4.7-12%, respectively. Analytical recoveries were 87-103%. Analysis of human plasma exposed to artificial oxidation with Cu(2+) ion and hydrogen peroxide, a free radical-generating reaction, showed marked increases in hydroxy and hydroperoxy PUFA concentrations. CONCLUSION: Lipid-derived hydroxy and hydroperoxy PUFAs may be useful as clinical markers of lipid peroxidation and oxidative stress in the peripheral circulation.

Chromatography, High Pressure Liquid↗

PubMed2002

Exposure of human neutrophils to oxygen radicals causes loss of deformability, lipid peroxidation, protein degradation, respiratory burst activation and loss of migration.

The effects of oxygen radical generating system of H(2)O(2) on neutrophil deformability, lipid peroxidation, protein degradation, chemotaxis, random migration and activation were studied in the presence and absence of selected anti-oxidants such as vitamin E and carbon monoxide. Hydrogen peroxide caused a significant loss of neutrophil deformability (measured as an index of filtration), loss of chemotaxis (using chemoattractant) and loss of random migration (spontaneous migration) under agarose gel. Hydrogen peroxide also caused a significant increase in lipid peroxidation (measured as malonyldialdehye) and protein degradation (measured as free alanine). Hydrogen peroxide also caused activation of neutrophils (measured by nitroblue tetrazolium dye test). Pre-incubation of neutrophils with vitamin E prevented significantly the increase in lipid peroxidation without affecting the loss of neutrophil deformability. However, pre-incubation with carbon monoxide prevented significantly the increase in protein degradation and the loss of neutrophil deformability. The results indicate the importance of oxidatively damaged cell proteins in compromising the rheologic behaviour and migration of neutrophils, particularly under oxidative stress conditions.

Antioxidants↗

PubMed1992

Studies of lipid peroxidation products in cerebrospinal fluid and serum in multiple sclerosis and other conditions.

Lipid peroxides were measured in cerebrospinal fluid (CSF) and sera from patients with multiple sclerosis (MS) or other conditions and from control subjects. In serum, visible fluorescence, A240nm, and free and protein-bound thiobarbituric acid (TBA)-reactive substances were significantly greater in MS patients than in control subjects. No such differences were observed in CSF. There was no correlation between lipid peroxides and disease severity or relapse time. We observed a significant positive correlation between CSF protein-bound TBA-reactive substances and CSF protein, suggesting that production of the former depends on protein concentration. A significant negative correlation between free TBA-reactive substances in serum and ultraviolet fluorescence indicated that production of free TBA-reactive substances may be associated with decreased production of fluorescent lipid peroxides. This study provides evidence for increased lipid peroxidation in serum but not CSF from MS patients, suggesting that either there is no increase in CSF lipid peroxidation in MS patients or that CSF lipid peroxides are rapidly removed, possibly by binding to CSF proteins that can be reabsorbed into the blood.

Adult↗

PubMed2005

[Accelerated senescence of fresh-cut Chinese water chestnut tissues in relation to hydrogen peroxide accumulation].

Accelerated senescence of fresh-cut Chinese water chestnut (CWC) tissues in relation to active oxygen species (AOS) metabolism was investigated. Fresh-cut CWC (2 mm thick) and intact CWC were stored at 4 degrees C in trays wrapped with plastic films. Changes in superoxide anion production rate, activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) were monitored, while contents of hydrogen peroxide, ascorbic acid, MDA as well as electrolyte leakage were measured. Fresh-cutting of CWC induced activities of SOD, CAT and APX to a certain extent (Fig. 2B and Fig. 3), but simultaneously stimulated superoxide anion production markedly (Fig. 2A), enhanced hydrogen peroxide accumulation and accelerated loss in ascorbic acid (Figs. 4 and 5), which resulted in increased lipid peroxidation indicated by malondialdehyde (MDA) content and electrolyte leakage (Fig. 1). Statistics analysis indicated that there was a significantly positive correlation among hydrogen peroxide accumulation, MDA content and electrolyte leakage (Table 1). Histochemical detection with 3, 3'-diaminobenzidine further demonstrated that hydrogen peroxide accumulation increased in fresh-cut CWC during storage (Fig. 5). AOS production rate and activities of SOD, CAT and APX changed little while no obvious hydrogen peroxide accumulation was observed, in intact CWC during storage.

Ascorbate Peroxidases↗

PubMed2005

[Determination of peroxides in environmental samples by high performance liquid chromatography with fluorescence detection].

A high performance liquid chromatographic (HPLC) method with fluorescence detection was developed for the determination of hydrogen peroxide and organic peroxides in environmental samples, and the method has been applied to peroxides detection in urban air and rain samples. The analytical sensitivity was improved. Post-column derivatization involved the oxidation of peroxides to a fluorescent dimer using p-hydroxyphenylacetic acid, a reaction catalyzed by hemin. The optimal excitation wavelength was 315 nm, while the emission wavelength was 400 nm. The temperature of the reaction coil was controlled at about 30 degrees C. Based on the ratio of signal to noise of 3, the detection limits were 4.0 x 10(-9) mol/L for hydroperoxide (H2O2), 4.1 x 10(-8) mol/L for methylhydroperoxide (MHP) and 6.7 x 10(-8) mol/L for ethylhydroperoxide (EHP) for aqueous samples. While the corresponding detection limits were 2.4 ng/m3 for H2O2, 35.2 ng/m3 for MHP, and 74.4 ng/m3 for EHP for air samples. Air samples were collected by Horibe cold trap at the temperature of about -90 degrees C. The results show that H2O2, hydroxymethyl hydroperoxide (HMHP), MHP, and EHP were the major peroxides in air, and that peroxyacetic acid (PAA) was occasionally detected. In rain samples, the two major peroxides were H2O2 and HMHP.

Chromatography, High Pressure Liquid↗

PubMed2006

[The present-day look at lipid peroxidation].

Lipid peroxidation occurs in physiological conditions and it consists in oxidation of polyunsaturated fatty acids, which are basic biological membrane components. There are two pathway of lipid peroxidation: nonenzymatic and enzymatic. Both of the processes result in generation of various reactive products. Nonenzymatic lipid peroxidation consists in free radical oxidation of polyunsaturated fatty acids while in enzymatic lipid peroxidation the generation of lipid hydroxyperoxides is achieved by insertion of an oxygen molecule at the active centre of lipoxygenase. In this manuscript mechanisms of two processes are described in details. We concentrate on final products of oxidation fatty acids: isoprostanes and neuroprostanes which are regarded as the most important biomarkers of lipid peroxidation as well as on the role of enzymes participating in enzymatic lipid peroxidation process. Moreover we discuss catalytic activity of glutathione peroxidases and transferases--enzymes preventing results of oxidation polyunsaturated fatty acids.

Aldehydes↗

PubMed1991

Comparison of production of volatile hydrocarbons by phenylhydrazine-induced peroxidation in rats chronically treated with lead.

We have studied the effect of a chronic pretreatment by lead on the peroxidation processes by measuring the production of the four main volatile hydrocarbons: ethane and pentane as index of lipid peroxidation; propane as marker of protein peroxidation and ethylene as index of both lipid and protein peroxidations. Our results have shown that: 1) lead alone did not increase the physiological formation of alkanes indicating that lead is not able per se to initiate the peroxidative processes; 2) after phenylhydrazine injection, lipid peroxidation makers were not modified, except pentane in male lead-treated rats. Conversely, ethylene and propane exhalation were increased 45 min after phenylhydrazine injection in lead-treated rats indicating a potentialisation of the oxidative effect of phenylhydrazine, mainly on proteins, by lead.

Animals↗