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PubMed1993

Continuous monitoring of lipid peroxidation by measuring conjugated diene formation in an aqueous liposome suspension.

A method is described for the direct and continuous monitoring of lipid peroxidation in an aqueous suspension of sonicated liposomes. By means of ultraviolet difference spectroscopy using tandem cuvettes, the formation of conjugated dienes during liposome peroxidation can be followed. Using this technique, the effect of the fatty acid composition of liposomes on lipid peroxidation can be studied. The results show that both the extent and the time scale of lipid peroxidation are influenced by the fatty acid composition of the phospholipid liposomes. This was confirmed also by other methods, such as measurement of the formation of lipid hydroperoxides and measurement of the decrease in polyunsaturated fatty acids. The advantage of the method described is the direct and continuous monitoring of phospholipid peroxidation in an aqueous environment, without subsampling and extraction of peroxidation products into organic solvents. Using this experimental approach based on difference spectra the contributions from changes in liposome, CuSO4 and H2O2 concentrations are canceled, thus improving sensitivity. The method can be employed for measuring the susceptibility to peroxidation of membrane phospholipids from fatty acid modified endothelial cells.

Chromatography, Gas↗
PubMed1998

Effect of the lipid peroxide reaction caused by repeated cold stress on cisplatin-induced nephrotoxicity.

The peroxide reaction in mouse kidney was examined in order to determine the relationship between the lipid peroxide reaction caused by SART (specific alternation of rhythm in temperature) stress and that caused by drug administration. After exerting SART stress for one wk on 6-wk-old male ddY mice (stress group), the peroxide reaction generated by the administration of a single dose of cis-diamminedichloroplatinum (cisplatin: CDDP, 10 mg/kg, i.p.) into SART-stressed mice (stress + CDDP group) was compared with the reaction of CDDP-administered nonstressed mice (CDDP group), saline-administered nonstressed mice (saline group), and saline-administered SART-stressed mice (stress + saline group). Lipid peroxidation in the kidneys was significantly higher in the stress group upon cessation of stress exertion than in the normal group. However, no significant difference in the lipid peroxide level after administration of CDDP was observed between the CDDP groups. The renal glutathione levels were significantly different between the CDDP groups and the saline administered groups. These results indicate that the peroxide reaction is generated in the kidneys by stress, but stress has no effect on the peroxide damage caused by CDDP administration. However, the contribution of stress to renal function impairment requires further evaluation.

Animals↗
PubMed1999

Heavy metals, lipid peroxidation, and ciguatera toxicity in the liver of the Caribbean barracuda (Sphyraena barracuda).

Human consumption of over 400 species of tropical fish containing polyether toxins (e.g. ciguatoxins, maitotoxins) causes ciguatera fish poisoning. The Caribbean barracuda (Sphyraena barracuda) is one of the most potent ciguatoxic fish. The objective of this study was to determine whether toxicity of 14 barracuda livers was correlated with lipid peroxidation. A significant correlation (p = 0.015, Pearson's correlation) between lipid peroxidation and toxicity of barracuda liver was found. Because iron and copper are well-known catalysts of hydroxyl radical production and lipid peroxidation in biological systems, the correlation between the concentrations of these metals in barracuda liver and lipid peroxidation and toxicity was also investigated. Cadmium was significantly correlated (p = 0.014) with the toxicity of barracuda livers. This study provides the first data concerning the concentration of iron, copper, and cadmium in the liver of the Caribbean barracuda. Of the three metals studied in barracuda liver, iron was the most abundant, followed by copper and cadmium. Lipid peroxidation was highly variable and detected in five (36%) of the liver samples. Lipid peroxidation was not statistically significantly correlated (p > 0.05) with concentrations of iron, copper, and cadmium in barracuda liver. Collectively, these findings provide additional evidence that lipid peroxidation can be a mechanistic component of ciguatera toxicity in the Caribbean barracuda.

Animals↗
PubMed1999

Oxidation of 2,4-dinitrophenol by hydrogen peroxide in the presence of basic oxygen furnace slag.

A treatment process was developed when basic oxygen furnace slag (BOF slag) and hydrogen peroxide were used to oxidize 2, 4-dinitrophenol from an aqueous solution. BOF slag, final waste slurry from steel making plants, contains about 12.5% by weight of ferrous oxide. In an acid solution, BOF slag can be dissociated to produce ferrous ions and react with hydrogen peroxide to produce hydroxyl radicals and oxidize 2,4-dinitrophenol. The results of the research demonstrated that the process had a significant capacity for oxidation of 2,4-dinitrophenol from the aqueous phase. Various factors critical to the oxidation of 2,4-dinitrophenol were studied, including hydrogen peroxide concentration, concentration of BOF slag, initial concentration of 2,4-dinitrophenol, and pH value of solution. Experimental results proved that 100 mg/L 2, 4-dinitrophenol and its oxidation intermediate could be totally decomposed within 60 min by 10 g/L BOF slag, 0.18 g/L hydrogen peroxide and pH 2.8 +/- 0.2. The optimum hydrogen peroxide concentration for degradation of 100 mg/L of 2,4-dinitrophenol is between 0.09 g/L and 0.18 g/L as 10 g/L BOF slag in the solution of pH 2.8 +/- 0.2. A hydrogen peroxide concentration higher than 0.18 g/L is disadvantageous to the oxidation process. The oxidation efficiency increased with the increase of BOF slag concentration at 0.18 g/L hydrogen peroxide dose. The best pH value of the solution is in the vicinity of 2.8. An oxidation reaction mechanism was proposed for predicting the concentration changes of 2, 4-dinitrophenol, ferrous ion, and hydrogen peroxide.http://link. springer-ny.com/link/service/journals/00244/bibs/37n4p427.++ +html</HEA

2,4-Dinitrophenol↗
PubMed2003

Application of postmortem lipid peroxidation in heart tissue to the diagnosis of myocardial damage.

The response by the myocardial tissue to injury may be manifested as macroscopical or microscopical lesions or, following an ischemia-reperfusion process, by the formation of reactive oxidant substances (ROS) which, in turn, may increase lipid peroxidation levels in myocardial tissue. The aim of this study was to determine whether the levels of lipid peroxidation in myocardial tissue from subjects who had died from different causes are related to cardiac lesions of ischemic or traumatic aetiology. We studied 825 hypostasis-free samples taken from the myocardial tissue of 75 cadavers. In all cases, a survival period was known to have existed. Lipid peroxidation in myocardial tissue was estimated by the colorimetric determination of malondialdehyde. The highest levels of tissue peroxidation were observed in the group of subjects who died from myocardial infarction. We observed a statistically significant correlation between the extent of peroxidation and the presence of myocardial damage of ischemic or traumatic aetiology. In our study, lipid peroxidation was associated with myocardial injury. The data suggest that the extent of lipid peroxidation in myocardial tissue may be used as a reliable indicator of myocardial damage in support of data obtained by conventional microscopy.

Adolescent↗
PubMed1997

An esterification protocol for cis-parinaric acid-determined lipid peroxidation in immune cells.

Loss of fluorescence from cis-parinaric acid (cPnA) is a sensitive indicator of lipid peroxidation. The purpose of this study was to utilize cPnA to determine, at the level of the intact immune cell, whether enrichment of membranes with polyunsaturated fatty acids (PUFA) increased lipid peroxidation. P388D1 macrophages were labeled by addition of cPnA as an ethanolic solution. Within two minutes of addition, in the absence-of serum, cPnA rapidly intercalated into the plasma membrane. Lipid peroxidation was initiated by addition of Fe(2+)-EDTA resulting in a dose-dependent decrease in fluorescence with increased oxidant concentration. Cells previously enriched with PUFA and labeled by intercalation showed no differences in spontaneous or Fe(2+)-induced lipid peroxidation. In separate experiments, 20 microM cPnA in ethanolic solution was injected into cell culture media containing 0.1% essentially fatty acid free bovine serum albumin (BSA). Cells were resuspended and incubated for 90 min at 37 degrees C. After washing with BSA to remove cPnA which had not incorporated, 0.5% (0.1 microM) of the added cPnA was found esterified within cellular lipids. This level of cPnA provided a 100-fold increase over basal autofluorescence levels. Cells labeled in this manner also lost fluorescence in a dose-dependent manner as levels of oxidant stress increased. Cells enriched with PUFA and labeled by esterification had significantly increased rates and total amounts of lipid peroxidation. Co-incubation with alpha-tocopherol and PUFA resulted in a decrease in lipid peroxidation which was not significantly different from control cells. In conclusion, esterification of cPnA into membrane phospholipids can sensitively detect changes in lipid peroxidation induced by alteration of membrane PUFA and/or vitamin E content.

Cells, Cultured↗
PubMed1997

Photo-initiated peroxidation of lipids in micelles by azaaromatics.

The monoazaaromatics, pyridine (1), hexyl nicotinate (2), and quinoline (3) and diazaaromatics, pyrimidine (4) and purine (5), readily act as photo-initiators for the peroxidation of methyl linoleate in 0.50 M SDS at 37 degrees C giving free radical chain oxidations of linoleate. Quantitative kinetic runs on the order in substate, RH, and in the rate of chain initiation, Ri, showed that the classical rate law for autoxidation, -d[O2]/dt = (kp/(2 kt 1/2))[RH] x Ri 1/2, is applicable to these photo-initiated oxidations. The oxidizability of methyl linoleate under these conditions is 2.92 x 10(-2) M-1/2 s-1/2. These peroxidations were inhibited by chromanol phenolic antioxidants of the vitamin E class, such as lipid-soluble 2,2,5,7,8-pentamethyl-6-hydroxychroman (PMHC) and water-soluble 2-carboxy- 2,5,7,8-tetramethyl-6-hydroxychroman (Trolox) and derived rate constants for inhibition of peroxidation were kinh (PMHC) = 4.35 x 10(4) M-1 s-1 and k(inh) (Trolox) = 2.81 x 10(4) M-1 s-1 during inhibited oxidation of methyl linoleate photo-initiated by 4. The products from photo-initiated peroxidation of methyl linoleate by 1 through 5 were determined by reduction and high-performance liquid chromatography analyses to be the 9- and 13-positional hydroperoxides of the four geometrical isomers: cis-9, trans-11 (6), trans-10, cis-12 (7), trans-9, trans-11 (8), and trans-10, trans-12 (9)-octadecadienoates typical of the free radical chain mechanism of lipid peroxidation. Products from dye-sensitized oxidation by Methylene Blue or Rose Bengal of methyl linoleate gave a product distribution of six hydroperoxides typical of oxidation by singlet oxygen. Thermal or photo-initiated peroxidation of methyl linoleate in SDS gave some selectivity of oxidation at the 13-position of the linoleate chain. The ratio of 13- to 9-oxidation varied in the range 1.23 to 1.14 as the cis/trans to trans/trans ratio of geometrical isomers varied from 0.44 to 1.25 during photooxidation of increased amounts of linoleate in SDS. This selectivity is attributed to loss of the pseudo symmetry around the pentadienyl system in the lipid chain in the SDS system during the peroxidation.

Antioxidants↗
PubMed1993

Lipid peroxides and antioxidant defenses in accelerated transplantation-associated coronary arteriosclerosis.

Accelerated coronary artery disease develops in most if not all heart transplant recipients within the first year after transplantation. Increased lipid peroxidation seems to be involved in atherogenesis. In these patients we have investigated whether there is an association between lipid peroxidation, reduced antioxidant defenses, and some conventional coronary risk factors. Lipid peroxides, lipids, uric acid, albumin, antioxidant enzymes and their cofactors (the trace elements selenium, iron, copper, and zinc) have been determined in heart transplant recipients compared with nonrecipients with coronary artery disease. Lipid peroxides (p = 0.002) and uric acid (p = 0.01) were higher and zinc (p = 0.001) was lower in heart transplant recipients. Thirteen of 30 transplant recipients compared with one of 30 nonrecipients (p < 0.001) had very low (less than 10 mumol/L) zinc levels. Antioxidant enzymes and other trace elements were not significantly different. In univariate regression analysis, zinc correlated positively with albumin (p = 0.02) and negatively with lipid peroxides (p < 0.05). Uricemia had a strongly positive correlation with hydroperoxides (r = 0.45; p = 0.0001). In stepwise multivariate regression analysis, lipids, uricemia, creatinine, and zinc were significant (p < or = 0.004) predictors of the lipid peroxide level. Cyclosporine and corticosteroid dosages were significant (p = 0.01) determinants of zinc concentration in the transplant recipients. Although a causal relationship between increased lipid peroxidation and accelerated arteriosclerosis is not definitely demonstrated, the results of this analysis suggest new insights into conventional coronary disease risk factors and possible therapeutic interventions; further controlled trials are needed.

Adult↗
PubMed1987

Quinone formation from carcinogenic benzo[a]pyrene mediated by lipid peroxidation in phosphatidylcholine liposomes.

The behavior of benzo[a]pyrene (B[a]P) during peroxidation of phosphatidylcholine (PC) liposomes initiated by an azo compound was investigated to examine the mechanism of quinone formation from carcinogenic B[a]P mediated by nonenzymatic lipid peroxidation occurring in vivo. B[a]P had a retarding effect on the peroxidation of polyunsaturated fatty acid moiety of PC. The major oxidation products which accumulated in the peroxidized liposomes were B[a]P 1,6-, 3,6-, and 6,12-quinone. Antioxidants acting as scavengers of chain-propagating lipid peroxy radicals effectively prevented not only lipid peroxidation but also B[a]P oxidation in the liposomal suspension. PC hydroperoxides, the primary products of PC oxidation, did not react with B[a]P in the absence of the azo compound, indicating that lipid peroxy radicals, not lipid hydroperoxides, are responsible for the formation of these quinones. The experiments using 18O2 gas and 18O-labeled methyl linoleate hydroperoxides demonstrated that B[a]P quinones are formed by incorporating molecular oxygen and their origin is partly due to the lipid peroxy radical. The mechanism proposed for the formation of B[a]P quinones mediated by peroxidation of membrane lipids involves a direct attack of the lipid peroxy radical on B[a]P and subsequent autocatalytic oxidation. Weak carcinogenic and noncarcinogenic pentacyclic aromatic hydrocarbons showed little reactivity to the lipid peroxy radical in the liposomes. Thus, the facility of the peroxidative attack on B[a]P may be related to the powerful carcinogenic activity of this substance.

Animals↗
PubMed1988

Increase of the molecular rigidity of the protein conformation in the intestinal brush-border membranes by lipid peroxidation.

The effect of lipid peroxidation on the protein conformation of the porcine intestinal brush-border membranes was studied using a fluorogenic thiol reagent, N-[7-dimethylamino-4-methylcoumarinyl]maleimide (DACM). By a kinetic analysis of the reaction of the membranes with DACM, it was shown that the reaction rate of the SH groups (SHf) of the membrane proteins, whose reaction with the dye is very fast, decreases in proportion to the extent of thiobarbituric acid-reactive substance formation. The difference in the rate of the reaction of the SHf groups for DACM between the control and peroxidized membranes completely disappeared after denaturation of the proteins by treatment with guanidine hydrochloride. The reaction of DACM with the SHf groups of the control membranes accelerated when the temperature was increased with an apparent transition temperature between 25 degrees C and 30 degrees C. On the other hand, no transition was observed in the peroxidized membranes over the temperature range 20-43 degrees C. These results suggest that the conformation around the SHf groups of the proteins in the peroxidized membranes is apparently different from that in the control membranes. A modification of the conformation around the SH groups in the membrane proteins associated with lipid peroxidation was further demonstrated by finding that the quenching efficiency of the fluorescence of the DACM-labeled membranes by Tl+ was markedly decreased after lipid peroxidation. Based on these results, changes in the protein conformation of the porcine intestinal brush-border membranes by lipid peroxidation are discussed.

Animals↗
PubMed1989

Cation transport in oxidant-stressed human erythrocytes: heightened N-ethylmaleimide activation of passive K+ influx after mild peroxidation.

Normal and chronically dehydrated (hereditary xerocytosis) human red cells were subjected to mild peroxidative treatment (315 microM hydrogen peroxide (H2O2), 15 min) in the presence of azide. The subsequent expression of passive (ouabain-resistant) K+ transport activities was analyzed by measurement of 86Rb+ influx. Peroxidation of normal red cells did not affect basal K+ transport activity, but the increment in K+ influx elicited by 0.5 mM N-ethylmaleimide (NEM) was increased 3-fold. The enhanced K+ influx was chloride-dependent, but only partially inhibited by 0.1 mM furosemide. Stimulated activity declined progressively after NEM activation, but could be restored by a second NEM treatment. Prior conversion of hemoglobin to the carbonmonoxy form abolished the response to peroxide, while 200 microM butylated hydroxytoluene (BHT) exerted only partial inhibition, suggesting that the effect of H2O2 requires interaction of activated, unstable hemoglobin species with the membrane, but that lipid peroxidation is not sufficient. Peroxidation following NEM treatment also enhanced NEM activation, indicating that enhancement does not require altered NEM reactions with stimulatory or inhibitory sites. Passive K+ transport in hereditary xerocytosis red cells was not activated by NEM, with or without H2O2 pretreatment. The results demonstrate that modest peroxidative damage to red cells can heighten the activation of a transport system that is thought to be capable of mediating net K+ efflux and volume reduction in cells that express it. Models are proposed in which the effects of NEM, H2O2, cell swelling and other factors are mediated by conformational changes in a postulated subpopulation of anion channel (Band 3) molecules that bind the K+ transporter.

Butylated Hydroxytoluene↗
PubMed1990

Differences in the susceptibility of plant membrane lipids to peroxidation.

Peroxidation of three membrane lipid preparations from plants was initiated using Fe-EDTA and ascorbate and quantified as the production of aldehydes and loss of esterified fatty acids. Using liposomes prepared from commercial soybean asolecithin, the degree of peroxidation was shown to be dependent on: the free radical dose, which was varied by the ascorbate concentration; the presence of tocopherol in the liposome; the configuration, of the liposome, multilamellar or unilamellar; and time after initiation. There were dramatic interactions among these factors which led to the conclusion that in comparing the susceptibility of different membrane preparations it is essential to examine the kinetics of the peroxidation reactions. The composition of the liposome was a major determinant of the degree of peroxidation and of the type of degradative reactions initiated by the oxygen free radicals. A fresh polar lipid extract from Typha pollen had very similar fatty acid composition to the soybean asolecithin, but was more resistant to peroxidation as shown by less aldehyde production and increased retention of unsaturated fatty acids after treatment. Similarly, microsomal membranes from the crowns of non-acclimated and cold acclimated winter wheat (Triticum aestivum L.) seedlings had a much higher linolenic acid content than soybean asolecithin but was much more resistant to peroxidation. In the winter wheat microsomes, the loss of esterified fatty acids was not selective for the unsaturated fatty acids; consequently, even with 40% degradation, the degree of unsaturation in the membrane did not decrease. These different reaction mechanisms which occur in plant membranes may explain why measurements of fatty acid unsaturation fail to detect peroxidative reactions during processes such as senescence, aging and environmental stress.

Aldehydes↗
PubMed1983

Inhibition of enzymic and non-enzymic lipid peroxidation of flounder muscle sarcoplasmic reticulum by pretreatment with phospholipase A2.

Sarcoplasmic reticulum, isolated from the muscle of winter flounder (Pseudopleuronectes americanus), was preincubated with phospholipase A2 to determine the effects of enzymic and non-enzymic lipid-peroxidation systems. Eicosapentaenoic acid (20:5) was preferentially released by phospholipase A2, but the percentage of docosahexaenoic acid (22:6) in the free fatty acids was similar to the percentage in membrane total fatty acids. A decrease in the production of both thiobarbituric acid-reactive substances and lipid hydroperoxides was observed in both the enzymic and non-enzymic peroxidation systems upon preincubation with phospholipase A2. Addition of palmitic acid or lysophosphatidylcholine did not inhibit either peroxidation system. Non-enzymic peroxidation was inhibited by the addition of beta-glycerophosphate, but enzymic peroxidation was apparently unaffected. A model is proposed to explain the inhibitory effect of phospholipid hydrolysis on lipid peroxidation in both systems, suggesting that fatty acids are structurally realigned upon hydrolysis, leading to decreased free-radical chain propagation. Additional factors appear to contribute to inhibition of enzymic peroxidation.

Animals↗
PubMed1985

Effect of dietary cholesterol on erythrocyte peroxidant stress in vitro and in vivo.

The effect of dietary variation of plasma cholesterol concentrations on the susceptibility of erythrocytes to in vitro and in vivo peroxidant stress was studied in rats. Malonyldialdehyde, produced in vivo (endogenous malonyldialdehyde) or following in vitro exposure of cells to 10 mM H2O2 (H2O2 malonyldialdehyde), was used as a measure of peroxidant stress. After 5 weeks, the plasma cholesterol concentrations in rats receiving 1.2% cholesterol + 0.6% cholic acid in their diet rose to 6-times that of control rats receiving a diet without added cholesterol; at the same time, erythrocyte H2O2 malonyldialdehyde in the cholesterol-fed rats decreased significantly relative to the control rats. During subsequent exposure of both groups to in vivo peroxidant stress with phenylhydrazine in two separate dose trials, erythrocyte peroxidant stress remained significantly lower in the cholesterol-fed rats: at a dose of 100 mumol/100 g body weight, H2O2 malonyldialdehyde was lower; at a dose of 25 mumol/100 g body weight, both endogenous and H2O2 malonyldialdehyde were lower. Erythrocyte membrane cholesterol concentrations were 12% higher in the cholesterol-fed rats than in controls. The effects of in vivo peroxidant stress on plasma cholesterol were also studied. In vivo peroxidant stress at the higher dose of phenylhydrazine produced a decrease in plasma cholesterol concentrations of control rats. The lower dose had no effect on this group and the plasma cholesterol concentrations were unchanged in the cholesterol-fed rats during both treatments. The data suggest that elevated plasma cholesterol concentrations are protective against erythrocyte peroxidant stress. The mechanism of cholesterol's protective effect is probably mediated through elevated membrane cholesterol concentrations.

Animals↗
PubMed1988

Relationship between mitochondrial lipid peroxidation and alpha-tocopherol levels in the guinea-pig adrenal cortex.

Lipid peroxidation in mitochondria from the functionally distinct inner (zona reticularis) and outer (zona fasciculata + zona glomerulosa) zones of the guinea-pig adrenal cortex was investigated. Ferrous ion (Fe2+)-induced lipid peroxidation was far greater in inner than outer zone mitochondria. Ascorbic acid similarly initiated lipid peroxidation to a greater extent in inner zone mitochondrial preparations. Differences in the unsaturated fatty acid content of inner and outer zone mitochondria could not account for the regional differences in lipid peroxidation. Total fatty acid concentrations were greater in the outer than in the inner zone, and the relative amounts of each fatty acid were similar in the two zones. However, mitochondrial concentrations of alpha-tocopherol, an antioxidant known to inhibit lipid peroxidation, were approx. 5-times greater in the outer than inner zone. The results demonstrate that there are regional differences in mitochondrial lipid peroxidation in the adrenal cortex which may be attributable to differences in alpha-tocopherol content. Thus, alpha-tocopherol may serve to protect outer zone mitochondrial enzymes from the consequences of lipid peroxidation and thereby contribute to some of the functional differences between the zones of the adrenal cortex.

Adrenal Cortex↗
PubMed1988

Monoclonal DLR1a/104G antibody recognizing peroxidized lipoproteins 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 (P3/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↗
PubMed1989

Nonesterified fatty acids inhibit iron-dependent lipid peroxidation.

The effect of various fatty acids on lipid peroxidation of liver microsomes induced by different methods in vitro was studied using oxygen uptake and malonaldehyde (MDA) production. It was observed that fatty acids with a single double bond are effective inhibitors of peroxidation. Stereo and positional isomers of oleic acid were equally effective as oleic acid. There was an absolute requirement for a free carboxyl group, since methyl esters of fatty acids and long-chain saturated and unsaturated hydrocarbons could not inhibit peroxidation. Saturated fatty acids with a chain length of 12-16 carbon atoms showed inhibition, whereas more than 18 carbon atoms reduced the inhibitory capacity. Fatty acids of lower chain length such as capric and caprylic acids did not show inhibition. Fatty acid inhibition was partially reversed by increasing the concentration of iron in the system. Peroxidation induced by methods which were independent of iron was not inhibited by fatty acids. It was observed that intestinal microsomes which were resistant to peroxidation due to the presence of nonesterified fatty acids in their membrane lipids were able to peroxidise by methods which do not require iron. These results suggest that certain fatty acids inhibit peroxidation by chelating available free iron. In addition, they may also be involved in competing with the esterified fatty acids in the membrane lipids which are the substrates for peroxidation.

Adenosine Diphosphate↗
PubMed1990

Cytochrome P-450 involvement in the NADPH-dependent lipid peroxidation in human placental mitochondria.

The NADPH-dependent lipid peroxidation in human placental mitochondria has been found to be inhibited strongly by amphenone B, aminoglutethimide and carbon monoxide, inhibitors of cytochrome P-450-mediated reactions, but was hardly affected by respiratory chain inhibitors. Cytochrome c, an exogenous electron acceptor which is known to compete with cytochrome P-450 for the reducing equivalents, showed an inhibitory effect on NADPH-dependent lipid peroxidation. The observed NADPH-dependent superoxide generation was also strongly inhibited by amphenone B and aminoglutethimide. Moreover, the lipid peroxidation in placental mitochondria was demonstrated to be stimulated by xanthine/xanthine oxidase added as superoxide generating system. This peroxidation was not affected by amphenone B and aminoglutethimide. On the other hand, the superoxide dismutase was found to inhibit both the xanthine oxidase- and NADPH-dependent lipid peroxidation. These data provide evidence that cytochrome P-450 is involved in NADPH-dependent mitochondrial lipid peroxidation. It is suggested that superoxide liberated from cytochrome P-450, in combination with iron, may be responsible for initiation of NADPH-dependent lipid peroxidation in human placental mitochondria.

Aminoglutethimide↗