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PubMed1977

Involvement of hydrogen peroxide in the regulation of senescence in pear.

Endogenous peroxide levels in pear fruit (Pyrus communis) were measured using a titanium assay method, and were found to increase during senescence in both Bartlett and Bosc varieties. Application of glycolic acid or xanthine, serving as substrates for the formation of H(2)O(2), increased the peroxide content of the tissue and accelerated the onset of ripening, as measured by increased softening and ethylene evolution. Application of ethylene also induced increased peroxide levels. Ripening processes were similarly promoted when peroxides were conserved by inhibiting the activity of catalase with hydroxylamine or potassium cyanide. By comparison, the inhibition of glycolate oxidase with alphahydroxy-2-pyridinemethanesulfonic acid decreased the peroxide content of the tissue and delayed the onset of ripening. These results indicate that the onset of ripening correlates with the peroxide content of fruit tissues as occurring under normal conditions or as influenced by the treatments. Hydrogen peroxide may be involved in oxidative processes required in the initiation and the promotion of ripening.

Journal Article↗
PubMed1991

Lipid peroxidation in peribacteroid membranes from French-bean nodules.

Enriched peribacteroid membranes were prepared from Phaseolus vulgaris nodules and, in the presence of metleghemoglobin and H(2)O(2), membranal lipid peroxidation was observed. The initial rate of the reaction was low and increased with time. Ferrous leghemoglobin was unable to induce this peroxidation with H(2)O(2). Thus, it appears that leghemoglobin (IV) is not the activated species involved in this process. Heme plays a role in this peroxidation and the hydroxyl radical is not an intermediate of the reaction. Lipid peroxidation in peribacteroid membranes was also observed in the presence of iron ions. A mixture of iron (III) and iron (II) produced a maximal peroxidation. Senescing nodule extracts were able to provoke membranal lipid peroxidation; they contained nonprotein-bound iron. Peribacteroid membranes were more sensitive than microsomes to peroxidation, as measured by malonaldehyde formation.

Journal Article↗
PubMed1990

Peroxidized lipoproteins recognized by a new monoclonal antibody (DLR1a/104G) in atherosclerotic lesions.

Monoclonal DLR1a/104G antibody, which recognizes peroxidized lipoproteins, was raised. Mice were immunized with the float-up fraction of the atherosclerotic arterial homogenate from WHHL rabbits. Sensitized spleen cells were fused with myeloma cells (3P/U1). Hybridoma clones were selected using peroxidized LDL prepared by CuSO4-catalyzed peroxidation and native LDL as positive and negative standards, respectively. The monoclonal DLR1a/104G antibody was highly reactive with peroxidized LDL, slightly with LDL modified with malondialdehyde, but not significantly with acetyl- or native LDL. The antigenicity in the case of peroxidized LDL did not decrease on extraction with hexane/isopropanol (3:2). The antigenicity coincided with the fluorescence (E350, F430) of the protein fraction of LDL peroxidized with CuSO4. These results suggest that an antigenic determinant exists in atherosclerotic lesions, which is the same as that for lipoproteins peroxidized with CuSO4.

Animals↗
PubMed1975

Singlet oxygen production associated with enzyme-catalyzed lipid peroxidation in liver microsomes.

Evidence for the formation of singlet oxygen during the oxidation of NADPH by liver microsomes is presented. The evidence is based primarily on the enzyme-dependent formation of dibenzoylethylene from diphenylfuran, a reaction which is specific for singlet oxygen. The apparent formation of singlet oxygen is coupled to the occurrence of peroxidation of microsomal lipid, a phenomenon known to be associated with NADPH oxidation by the particles. Both the peroxidation of lipid and the apparent formation of singlet oxygen are related to the amount of Fe3+ present in the system and the results are consistent with the possibility that the singlet oxygen formed by this system is derived from the breakdown of lipid peroxides. If 1O2 is formed from breakdown of lipid peroxides, it would be dependent on O-/-2 formation because superoxide anion has been shown to undergo reactions in this system which generate extremely reactive free radicals (probably hydroxyl) that initiate lipid peroxidation. These peroxides are quite unstable and their degradation may be the source of 1O2. We have consistently observed that O-/-2 itself is not a reactive radical with respect to lipids or radical scavengers. Hence, O-/-2 cannot be the radical which initiates lipid peroxidation on which 1O2 generation appears to depend. The results may offer at least part of the explanation for the dietary requirement for alpha-tocopherol which not only scavenges free radicals but quenches singlet oxygen as well. This report also includes description of studies indicating that another enzyme, xanthine oxidase, which forms superoxide anion during its activity under aerobic conditions, does not form singlet oxygen during its function. This finding is in contrast to reports of others which indicate that xanthine oxidase activity does produce 1O2.

Aniline Compounds↗
PubMedDate not supplied

Evaluation of lipid peroxidation in red blood cells by monitoring the uptake of sucrose and phenol red.

Red blood cells (RBCs) are prone to lipid peroxidation by virtue of their function as oxygen carriers, and also because of their lipid composition. Malondialdehyde (MDA) content using thiobarbituric reagent is widely used to quantify lipid peroxidation. In this study we compare MDA assay with a newly developed assay that evaluates the uptake of sucrose and phenol red into RBCs under peroxidative stress. Both sucrose and phenol red uptake show significantly higher correlation with incubation time compared with MDA assay. Furthermore, phenol red uptake into RBCs on treatment with H(2)O(2) has a direct linear proportional relationship, whereas it is hyperbolic with MDA. The assay also clearly shows that uptake of sucrose or phenol red is specific for intact cells (RBCs) prior to hemolysis. Assay validation is carried out by using known lipid peroxidation-causing agents, such as ferrous ions, and also by using peroxidation inhibitors such as alpha-tocopherol. This new method can be applied efficiently to evaluate lipid peroxidation in RBCs as well as other cells and tissues.

Absorption↗
PubMedDate not supplied

Hydrogen peroxide permeation across liposomal membranes: a novel method to assess structural flaws in liposomes.

Hydrogen peroxide permeation across large multilamellar vesicles of defined and complex lipid composition was shown to obey precise kinetic relationships for the activity of the occluded catalase. Careful assay conditions precluded simultaneous peroxidative damage to the lipids. The kinetic data was consistent with a barrier role for the bilayer for hydrogen peroxide permeation. More interestingly, hydrogen peroxide permeation across liposomes of complex lipid mixtures exhibited osmotic inhibition of permeation of hydrogen peroxide. On the other hand, purified egg lecithin vesicles did not exhibit any effect of external osmolality on hydrogen peroxide permeation in an experimentally defined non-lytic zone of external osmolarity. These results argue in favour of a heterogeneous, heteroporous structure of bilayers with complex lipid composition.

Animals↗
PubMed1993

Effect of bacterial lipopolysaccharide on the content of lipid peroxidation products in lungs and other organs of mice.

The influence of lipopolysaccharide from Escherichia coli (LPS, 17 mg/kg body weight) on the lipid peroxidation process in organs of mice was studied. The content of conjugated dienes (CD), lipid peroxides (LP), malondialdehyde (MDA) (all three lipid peroxidation by-products), peroxidase (PO) activity and wet-to-dry weight ratio in lungs, heart, spleen, kidneys and liver were determined 1.5 h after intravenous injection of LPS. Animals observed at this time-point had reduced activity and decreased body temperature by about 2 degrees C, however, all analysed organs did not reveal any changes of wet-to-dry weight ratio comparing to organs from mice injected with sterile, pyrogen free 0.9% NaCl. Only extracts from heart and lungs showed significant increase in the tissue level of at least two lipid peroxidation products. The heart content of CD, MDA, and LP was about 1.5-, 1.3-, and 2.4-fold higher than in control group. In lungs CD and MDA increased 3.3- and 1.3-times but in spleen only content of LP was elevated. In these organs the suppression of PO activity was also observed. Liver and kidneys did not reveal any convincing enhancement of lipid peroxidation process and alterations of PO activity. Since free radical reactions are involved in lipid peroxidation process and inactivation of PO these results suggest that heart, lungs and spleen are the organs mostly exposed to oxidative stress during the first 1.5 h after single injection of LPS in mice.

Animals↗
PubMed1995

Protection of cultured rat gastric cells against oxidant stress by iron chelation. Role of lipid peroxidation.

Reactive oxygen metabolites may be involved in the pathogenesis of ethanol-, nonsteroidal antiinflammatory drug-, Helicobacter pylori-, or ischemia/reoxygenation-induced gastric mucosal injury in vivo. Iron plays a critical role in mediating oxidant injury in vitro. The present study examined a possible role of lipid peroxidation in inducing oxidant damage by determining the effect of iron chelation on cytotoxicity and on lipid peroxidation in cultured rat gastric cells. Cytotoxicity was quantified by 51Cr release from prelabeled cells that were exposed to tert-butyl hydroperoxide (tBHP) so as to overwhelm the glutathione redox cycle. Lipid peroxidation was assessed by measuring malondialdehyde (MDA) production. tBHP caused a time-related and dose-dependent increase of 51Cr release. The presence of phenanthroline (a chelator of Fe2+) during tBHP exposure and pretreatment with deferoxamine (a chelator of Fe3+) reduced tBHP-induced 51Cr release dose dependently. The generation of MDA increased as the concentrations of tBHP increased, but in a time course study, such generation preceded cytolysis. Both iron chelators attenuated MDA production in a dose-dependent fashion. Oxidant stress causes lipid peroxidation in cultured gastric cells, which is then followed by cytolysis. Iron plays a critical role in inducing lipid peroxidation as well as in mediating cytolysis. Iron chelation protects these cells from oxidant stress presumably through inhibition of lipid peroxidation.

Animals↗
PubMed1996

Protection by multiple antioxidants against lipid peroxidation in rat liver homogenate.

The purpose of this study was to test the hypothesis that multiple antioxygenic nutrients provide increased protection against lipid peroxidative damage to rat liver. Rats were fed diets (i) deficient in vitamin E and selenium (Diet 1), (ii) supplemented with vitamin E and selenium (Diet 2), (iii) supplemented with (ii) and in addition trolox C, N-acetylcysteine, coenzyme Q0, and (+)-catechin (Diet 3), or (iv) supplemented with (iii) and in addition beta-carotene, ascorbic acid palmitate, canthaxanthin, and coenzyme Q10 (Diet 4). Liver homogenates were obtained from three rats fed each of the diets for six weeks and were incubated at 37 degrees C up to two hours with and without exogenous tertiary-butyl hydroperoxide (TBHP) or Cu2+. Lipid peroxidation was determined by measurement of thiobarbituric acid substances. Diets 2 and 3 significantly protected against in vivo hepatic lipid peroxidation, and this protection was augmented by Diet 4. Diets 2, 3, and 4 were protective against mild oxidation induced by TBHP or Cu2+. During incubations with exogenous TBHP and Cu2+, there were only small differences between diets supplemented with antioxidants in inhibition of lipid peroxidation, indicating that diets supplemented with vitamin E and selenium (Diet 2) may have provided the maximal protection for liver. The possible mechanisms of protection provided by multiple antioxidants in diets were discussed. Protection by multiple antioxidants against lipid peroxidation may translate to prevention of peroxidative damage to human tissue, a factor in human disease.

Animals↗
PubMed1991

Lead-induced tissue fatty acid alterations and lipid peroxidation.

Previous work showed that dietary lead (Pb) increases the relative concentration of arachidonic acid (20:4) as a percentage of total fatty acids, and decreases the relative proportion of linoleic acid (18:2) to arachidonic acid (18:2/20:4) in chick liver, serum, and erythrocyte membranes. The present investigation was undertaken to examine the time-course and magnitude of the fatty acid alterations with increasing dietary Pb levels. We also examined the effects of Pb on the fatty acid composition and lipid peroxide content of hepatic subcellular organelles. In Exp. 1, chicks were fed diets containing 0, 62.5, 125, 250, 500, or 1000 ppm added Pb (as Pb acetate trihydrate) from 1 to 21 d of age. After 21 d, no growth effects were observed; however, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver and serum lipids, and in total hepatic phospholipids in a dose-dependent manner. Hepatic mitochondrial membrane fatty acids were not altered, nor was there any increase in hepatic lipid peroxidation. In Exp.2, chicks were fed diets containing 0, 500, 1000, or 2000 ppm added Pb from 1 to 21 or 22 d of age. Pb depressed growth in a dose-dependent manner. In addition, Pb lowered the 18:2/20:4 ratio and increased 20:4 concentration in total liver lipids and in hepatic mitochondrial and microsomal membranes in a dose-dependent manner. Total hepatic lipid peroxidation was increased over control values by 1000 ppm Pb, and hepatic microsomal lipid peroxidation was increased by dietary Pb levels of 1000 and 2000 ppm. In Exp. 3, body weight, hepatic microsomal lipid peroxidation, and fatty acid composition were determined in 4-, 9-, 14-, 18-, and 23-d-old chicks fed 0 or 1500 ppm added Pb. Body weights of Pb-treated chicks were significantly lower than those of control chicks by day 18. Microsomal 20:4 concentration and peroxidation increased, and the 18:2/20:4 ratio decreased with age in both groups, but the changes were of greater magnitude in the Pb-treated chicks. The results suggest that some of the manifestations of Pb toxicity may be a reflection of increased concentration of 20:4 in specific membranes. Further, since the Pb-induced alterations in fatty acid composition were noted in the absence of any growth depression, we propose that fatty acid composition is more sensitive than growth rate to the presence of lead in the diet.

Animals↗
PubMed1999

Modulation of antioxidant enzymes and lipid peroxidation in salivary gland and other tissues in mice by moderate treadmill exercise.

The current experiments were designed to study the effect of moderate treadmill training exercise on lipid peroxides and antioxidant enzyme activity in various tissues of ICR mice. Three-month-old female mice were trained on a treadmill to run daily from 45 to 50 minutes, at 1 km per hour, 6 days a week for a total of 8 weeks. At the end of the 8-week endurance-training period, both sedentary control (SC) and exercise-trained (ET) mice were sacrificed, and various tissues were collected to measure antioxidant enzyme activity. The results showed weight gain and serum lipid peroxides significantly decreased in ET mice compared to SC mice. Also, although lipid peroxide levels in kidney and salivary glands were found to be significantly decreased in ET mice, these mice showed higher lipid peroxide levels in the liver compared to SC mice. No change was observed in heart and calf muscle tissue of the ET mice. Exercise was also noted to increase superoxide dismutase (SOD) activity in kidney, heart, and calf muscle homogenates. Increases in catalase activity were present in liver, heart, calf muscle, and salivary gland homogenates of ET mice compared to their SC counterparts. Exercise was also shown to increase glutathione peroxidase activity in liver, kidney, and heart homogenates, as well as glutathione transferase activity in liver and salivary gland homogenates. In addition, exercise training was found to increase reduced and total glutathione levels in heart, calf muscle, and salivary gland. These results indicate that moderate exercise is beneficial to the lowering of lipid peroxides and the increasing of antioxidant enzyme activity specifically in the salivary gland, and also in various organs. However, its beneficial effect on elevation of antioxidant enzymes and suppression of lipid peroxide, varies from organ to organ.

Animals↗
PubMed1997

Lipid peroxidation during n-3 fatty acid and vitamin E supplementation in humans.

The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake, alone or in combination with dL-alpha-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eighty men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n-3 fatty acids) or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde (MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was measured. Plasma alpha-tocopherol concentration increased in those receiving vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids, EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma MDA and lipid peroxides increased (P < 0.001 and P < 0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n-3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation.

Adult↗
PubMed1988

Vanadium and lipid peroxidation: evidence for involvement of vanadyl and hydroxyl radical.

The present study was designed to determine which form of vanadium is involved in initiating conjugated diene formation in both purified and partially peroxidized fatty acids, and to determine if active oxygen radicals are involved in this process. We report that vanadyl is the active form of vanadium in initiating conjugated diene formation in micelles prepared from purified fatty acids or partially peroxidized fatty acids. Vanadate did not initiate conjugated diene formation in either case. Hydroxyl radicals were shown to be involved in the initiation of diene conjugation when vanadyl and hydrogen peroxide were added together in a reaction mixture. In this case, there was a rapid burst of conjugated diene formation which quickly leveled off. Using spin trapping techniques, hydroxyl radicals were shown to be generated in the vanadyl-catalyzed break-down of fatty acid hydroperoxides. A comparison was made between the ability of vanadyl or vanadyl chelates to decompose hydrogen peroxide and catalyze the decomposition of fatty acid hydroperoxides. It was found that strongly chelated vanadyl (vanadyl/EDTA) was much less effective in decomposing both hydrogen peroxide and fatty acid hydroperoxides than the weak vanadyl chelates (e.g., vanadyl/ADP). This study suggests a mechanism to explain the effects of vanadium on lipid peroxidation.

Electron Spin Resonance Spectroscopy↗
PubMed1988

Site-specific induction of lipid peroxidation by iron in charged micelles.

Generation of hydroxyl radicals by the Fenton reaction resulted in lipid peroxidation of linoleic acid (LA) (H2O2-Fe2+-induced lipid peroxidation) in positively charged tetradecyltrimethylammonium bromide (TTAB) micelles, but not in negatively charged sodium dodecyl sulfate (SDS) micelles. However, more OH radicals formed via the Fenton reaction were trapped by N-t-butyl-alpha-phenylnitrone (PBN) in SDS micelles than in TTAB micelles. When detergent-dispersed LA was contaminated with linoleic acid hydroperoxide (LOOH), lipid peroxidation was catalyzed by Fe2+ via reductive cleavage of LOOH (LOOH-Fe2+-induced lipid peroxidation), and Fe2+ was oxidized simultaneously in SDS micelles, even when H2O2 was not present. In contrast, LOOH-Fe2+-induced lipid peroxidation and simultaneous oxidation of Fe2+ were not observed in TTAB micelles. An ESR spectrum presumed to be due to an alkoxy radical trapped by PBN was also detected in SDS micelles, but not in TTAB micelles in the LOOH-Fe2+-induced lipid peroxidation system. The results are discussed in the light of the localization of iron, the unsaturated bonding moiety of LA, the OOH-group of LOOH, and the trapping site of PBN in different charged micelles.

Arachidonic Acid↗
PubMed1990

Peroxidation-induced perturbations of erythrocyte lipid organization.

Peroxidation of erythrocyte membrane lipids by hydrogen peroxide perturbs the lipid bilayer and increases phagocytosis by macrophages. This study addresses the underlying mechanism of these processes, and in particular the role of malondialdehyde, a major byproduct of lipid peroxidation. When erythrocytes were treated with hydrogen peroxide or ascorbate/iron to generate malondialdehyde, or with malondialdehyde itself, only those cells treated with hydrogen peroxide showed increased phospholipid spacing and enhanced phagocytosis. This result indicates that the alterations observed are unique to hydrogen peroxide treatment, and that malondialdehyde does not play a role in inducing these changes in surface properties. Comparison of adherence to human umbilical vein endothelial cells and phagocytosis showed that increased phagocytosis was not mirrored by enhanced adherence. This result suggests that two different signals may mediate recognition of erythrocytes by macrophages and by endothelial cells.

Cell Adhesion↗
PubMed1990

Lipid peroxidation in rat liver microsomes. II. Response of hydroperoxide formation to iron concentration.

When rat liver microsomes were incubated with NADPH, the major products were hydroperoxides which increased with time indicating that endogenous iron content is able to promote lipid peroxidation. The addition of either 5 microM Fe2+ or Fe3+ ions strongly enhanced the hydroperoxide formation rate. However, due to the hydroperoxide breakdown, hydroperoxide concentration decreased with time in this case. Higher ferrous or ferric iron concentration did not change the situation much, in that both hydroperoxide breakdown and formation were similar to those when NADPH only was present in the incubation medium. After lipid peroxidation, analysis of fatty acids indicated that the highest amount of peroxidized PUFA occurred in the presence of 5 microM of either Fe2+ or Fe3+. This analysis also showed that after 8 min incubation with low iron concentration, PUFA depletion was about 77% of that observed after 20 min, whereas without any iron addition or in the presence of 30 microM of either Fe3+, PUFA decrease was only about 37% of that observed after 20 min. As far as the optimum Fe2+/Fe3+ ratio required to promote the initiation of microsomal lipid peroxidation in rat liver is concerned, the highest hydroperoxide formation was observed with a ratio ranging from 0.5 to 2. These results indicate that microsomal lipid peroxidation induced by endogenous iron is speeded up by the addition of low concentrations of either Fe2+ or Fe3+ ions, probably because free radicals generated by hydroperoxide breakdown catalyze the propagation process. In experimental conditions unfavourable to hydroperoxide breakdown the principal process is that of the initiation of lipid peroxidation.

Adenosine Diphosphate↗
PubMed1990

Polychlorinated biphenyls-induced lipid peroxidation as measured by thiobarbituric acid-reactive substances in liver subcellular fractions of rats.

Rats were given a 0.05% polychlorinated biphenyls (PCB) diet supplemented with adequate nutrients for 10 days and not only PCB-induced lipid peroxidation as measured by thiobarbituric acid (TBA)-reactive substances but also variations of lipid peroxides scavengers in liver and its subcellular fractions (nuclei and cell debris, mitochondrial, microsomal and cytosolic fractions) were investigated. The lipid peroxidation in liver and subcellular fractions in the PCB-treated group increased significantly except in the nuclei and cell debris fraction. The increase in lipid peroxidation in the microsomal fraction appeared to be associated in part with the decrease in vitamin E (alpha-tocopherol) content and induction of drug-metabolizing enzymes. In the cytosolic fraction, the total lipid content increased, glutathione peroxidase (GSHPx) activity decreased and the quantity of free radical-reactive substances suppressing lipid peroxidation was low as measured by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) value. From these results, the increase in lipid peroxidation in the cytosolic fraction in the PCB-treated group was ascribed to the abundance and availability of oxidizable substrate attended with fatty liver, to the decline in GSHPx activity, and to the insufficiency in antioxygenic activity as observed by the decrease in the DPPH value.

Animals↗
PubMed1985

Decreased susceptibility of red blood cells to lipid peroxidation in patients with alcoholic liver cirrhosis.

Red blood cells from alcoholics with and without liver cirrhosis and control subjects were examined for the susceptibility to lipid peroxidation. Red blood cells of patients with liver cirrhosis were found to be less sensitive to hydrogen peroxide-induced peroxidation measured by a new, reliable and sensitive method: the release of pentane during red blood cell lipid peroxidation. Changes of sensitivity to lipid peroxidation correlated with the severity of the liver malfunction, but not with abnormalities of the lipid composition of red cell membranes which are apparent in patients with liver disease. In alcoholics without liver cirrhosis, only minor changes in the susceptibility of red cells to peroxidation were observed.

Erythrocytes↗