Decomposition Of Linoleic Acid Hydroperoxide Research Articles

Phytic Acid Inhibits Lipid PeroxidationIn Vitro

Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation under in vitro and in vivo conditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10–20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products.

Formation of Superoxide Anion during Ferrous Ion-Induced Decomposition of Linoleic Acid Hydroperoxide under Aerobic Conditions

We studied the mechanism of formation of oxygen radicals during ferrous ion-induced decomposition of linoleic acid hydroperoxide using the spin trapping and chemiluminescence methods. The formation of the superoxide anion (O2*-) was verified in the present study. The hydroxyl radical is also generated through Fenton type decomposition of hydrogen peroxide produced on disproportionation of O2*-. A carbon-centered radical was detected using 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline N-oxide (DEPMPO) as a spin trap. Alkoxyl radical formation is essential for the conversion of linoleic acid hydroperoxide into the peroxyl radical by ferrous ion. It is likely that the alkoxyl radical [R1CH(O*)R2] is converted into the hydroxylcarbon radical [R1C*(OH)R2] in water, and that this carbon radical reacts with oxygen to give the alpha-hydroxyperoxyl radical [R1R2C(OH)OO*], which decomposes into the carbocation [R1C+(OH)R2] and O2*-.

Potential role of conjugated bilirubin and copper in the metabolism of lipid peroxides in bile.

Conjugated bilirubin and copper ions at their physiological concentrations in bile may play an important role in hydroperoxide and other detoxification. Conjugated bilirubin may also be an important chain-breaking antioxidant preventing lipid peroxidation. Bilirubin ditaurine (BR-DT), a water-soluble model compound of conjugated bilirubin, completely prevents the peroxyl radical-induced oxidation of phosphatidylcholine in either multilamellar liposomes or micelles. This antioxidant activity is associated with the bilirubin moiety of BR-DT, since taurine alone is inefficient in scavenging peroxyl radicals. The number of peroxyl radicals trapped per molecule of BR-DT is 1.9, compared to 4.7 trapped per molecule of biliverdin, the water-soluble physiological precursor of bilirubin. Peroxyl radical-induced oxidation of BR-DT results in a spectral shift in maximal absorbance toward shorter wavelengths; biliverdin is not formed as a major oxidation product. BR-DT, but neither taurine nor biliverdin, greatly accelerates the cupric ion-catalyzed decomposition of linoleic acid hydroperoxide. In the presence of ferric ion, BR-DT shows no lipid hydroperoxide-degrading activity. Addition of cupric ion to BR-DT results in formation of a complex with spectral features similar to that of a biliverdin-cupric ion complex, indicating that BR-DT and cupric ion undergo redox reactions.

Negative ames tests of epoxide fatty methyl esters derived from homolysis of linoleic acid hydroperoxides

Five isomeric epoxyhydroxyene and epoxyoxoene fatty esters derived from homolytic decomposition of linoleic acid hydroperoxide were tested for mutagenicity by the ‘Ames’ top-agar incorporation method using S-9 mix derived from livers of male rats pretreated with Aroclor 1254. The epoxide fatty esters tested—methyl trans-12,13-epoxy- erythro-11-hydroxy- cis(trans)-9-octadecenoate and methyl trans-12,13-epoxy- threo-11-hydroxy- cis(trans)-9-octadecenoate (each composed of approximately 80% cis-9-ene and 20% trans-9-ene), methyl trans-12,13-epoxy-9-oxo- trans-10-octadecenoate, methyl trans-12,13-epoxy-9-hydroxy- trans-10-octadecenoate and methyl cis-12,13-epoxy-9-oxo- trans-10-octadecenoate—had structural characteristics similar to certain potent mutagens. However, these ester were not mutagenic in Salmonella typhimurium strains TA 100, TA98 or TA1537 at concentrations up to 2000 μg/test plate. Under the same test conditions, the methyl ester of hydroperoxy linoleic acid, from which these epoxides were derived, was weakly mutagenic in strain TA100 and possibly also in strain TA98.

Decomposition of linoleic acid hydroperoxides

Methyl 13-hydroperoxy-cis-9-trans-11-octadecadienoate (13-HPODMe) was incubated with ditert-butyl peroxyoxalate or copper(II)palmitate for 3 h at 38 °C. Numerous products were identified and quantitatively analysed. The chemical structures and the amount of products resulting from the 13-HPODMe/Cu(pal)2 system were influenced by both the presence of oxygen and the addition of some antioxidants (α-,γ-,δ-tocopherols, ascorbyl palmitate).

Effect of autoxidized oil on carp - II. Decomposition of linoleic acid hydroperoxide in carp intestine.

To clarify the toxic effect of lipid hydroperoxides on fish, the decomposition process of lipid hydroperoxides in carp intestinal tissue was studied. Pure linoleic acid hydroperoxide was incubated with carp intestinal extract or acetone powder, and the decomposition rate of hydroperoxide and the formation of carbonyl compounds were investigated. To determine the degree of involvement of the enzymatic reaction in the decomposition of hydroperoxides, the data was compared with the control system which was incubated with the boiled intestinal preparation. In addition, the inhibitory effect of EDTA and cyanide was also investigated to examine the influence of metal ions and heme compounds on the reaction. As a result, both the systems decomposed approximately equivalent amount of hydroperoxide and carbonyl compounds, specially unsaturated carbonyls were elevated more in the experimental system than in the control. This result was supported by a higher UV absorption at 275nm of the experimental system. Both EDTA and cyanide have only a partial inhibitory effect on the reaction. These data indicate that most of the lipid hydroperoxides were decomposed in carp intestinal tissue and converted to carbonyl compounds. It was suggested that heat-unstable substances in the carp's intestine were partly involved in the formation of unsaturated carbonyls from lipid peroxides.

Volatile hydrocarbon and carbonyl products of lipid peroxidation: a comparison of pentane, ethane, hexanal, and acetone as in vivo indices.

A study was undertaken to determine whether respiratory hexanal and acetone as well as pentane and ethane could be measured as potential indices of lipid peroxidation in vivo. The tests of induction of lipid peroxidation in rats included injection of iron-dextran and the vitamin E deficiency status. Injection of 460 mg of iron/100 g body wt over a 28-day period increased pentane and ethane production 4- and 6-fold, respectively. Hexanal production was increased 7-fold after injection of 60 mg of iron/100 g body wt, and then it fell back to the preinjection level in spite of continued injection of iron-dextran. Acetone production was lower in iron-injected rats than in controls, and it was ca. 10-fold higher in fasted vitamin E-deficient rats than in vitamin E-supplemented rats, being ca 48 and 5 nmol/100 g/min, respectively. It was observed that halomethane injection did not increase hexanal production, while acetone and pentane production were increased. Pentane and hexanal, but not acetone, were found to arise from decomposition of linoleic acid hydroperoxide in vitro. It was concluded that hydrocarbon gases are better indices of lipid peroxidation than hexanal, which is enzymatically metabolized, and acetone, the production of which is dominated by factors such as altered carbohydrate metabolism.

Decomposition of linoleic acid hydroperoxides by radicals

Methyl 13-hydroperoxy-cis,trans-9,11-octa-decadienoate (LMPO) was incubated with di-t-butyl peroxyoxalate for 3 h at 38 °C. In the presence of oxygen LMPO decomposed to numerous products among which were methyl 13-oxo-trans,trans-9,11- and methyl 9-oxo-trans,trans-10,12-octadecadienoate, methyl 13-oxo-trans-9,10-epoxy-trans-11-and methyl 9-oxo-trans-12,13-epoxy-trans-10-octadecenoate, methyl 9-hydroxy-trans-12,13-epoxy-trans-10-and methyl 13-hydroxy-trans-9,10-epoxy-trans-11-octadecenoate. Flushing the reaction system with nitrogen reduced the breakdown of LMPO and altered the reaction route in such a manner that a dimethyloctadecadienoate peroxide appeared as the major product.

Effects of amino acids on the photosensitized oxidation of linoleic acid in an aqueous ethanol solution.

The antioxidative activities of l-amino acids on the methylene blue sensitized photooxidation of linoleic acid (LA) were studied in a 40% aqueous ethanol solution at pH 7.0 and 33°C. His and CysH inhibited the photosensitized oxidation of LA, and the antioxidative activity of His was larger than that of CysH. The ratio of the chemical reaction rate constant for His and singlet oxygen (1O2) to that for LA and 1O2 was similar to the ratio of the 1O2 quenching rate constant for His to that for LA. This fact shows that His inhibits the photosensitized oxidation of LA by quenching 102 chemically.On the other hand, CysH reacted with linoleic acid hydroperoxides (LAHPO) or with and caused the decomposition of LAHPO or the formation of Cys. This fact suggests that CysH inhibits the photosensitized oxidation of LA by decomposing LAHPO or by quenching 1O2 chemically.

Evidence for generation of O2- or an O2--like factor in the decomposition of linoleic acid hydroperoxide.

Evidence for generation of O2- or an O2--like factor in the decomposition of linoleic acid hydroperoxide.

Studies on Metal-Protein Complex. XII.

The effects of proteins and peptides on catalytic autoxidation of linoleic acid (LA) by Cu (II) were investigated in an aqueous ethanol solution at pH 7.0 and 35°C in the dark. Proteins and peptides of molecular weight above 600 formed the insoluble complexes with cupric ion and inhibited the catalytic autoxidation of LA by Cu (II). Dipeptides and peptides of molecular weight 200 formed the soluble complexes with cupric ion and promoted the catalytic autoxidation of LA by Cu (II). In general, the prooxidant effects of Cu (II) -acidic or neutral dipeptide complexes were proportional to the catalytic reactivities of the complexes on the decomposition of linoleic acid hydroperoxide (LAHPO). The above facts suggest that the soluble complexes, except Cu (II) -basic dipeptide complexes, promote the radical formation by decomposing LAHPO, and that the insoluble complexes deactivate the catalytic reactivity of cupric ion by confining the ion in the complex.

Chlorophyll destruction in the presence of bisulfite and linoleic acid hydroperoxide

Chlorophyll was rapidly destroyed in the presence of bisulfite and linoleic acid hydroperoxide. Both bisulfite and linoleic acid hydroperoxide were required for chlorophyll destruction and both were consumed in the reaction; however, there was no oxygen requirement. Chlorophyll destruction occurred most readily in the slightly acidic pH region with little destruction occurring above pH 8. The free radical scavengers, hydroquinone and α-tocopherol, were very effective at inhibiting chlorophyll destruction, but the singlet oxygen quenchers, β-carotene, 2,5-dimethylfuran and 1,3-diphenylisobenzofuran, were only slightly effective. The addition of metal chelators indicated that metals were not participating in the reaction. The evidence indicates that chlorophyll was destroyed by a free radical mechanism. Based on the present results and that of others, it is suggested that chlorophyll was destroyed via oxidation by the alkoxy radical which was produced during the decomposition of linoleic acid hydroperoxide by bisulfite.

Oxygenated fatty acid constituents of soybean phosphatidylcholines.

AbstractBitter‐tasting phosphatidylcholines from hexane‐defatted soybean flakes were chromatographically separable from ordinary soy phosphatidylcholines (SPC). The bitter‐tasting SPC contain 32% oxygenated fatty acids in addition to palmitic, stearic, oleic, linoleic, and linolenic acids. Identification of these oxygenated acids was based on infrared, ultraviolet, proton nuclear magnetic resonance, and mass spectral characteristics of methyl ester derivatives which were separated and purified by column and thin layer chromatography. The fatty acid methyl esters identified were (a) 15, 16‐epoxy‐9, 12‐octadecadienoate, (b) 12, 13‐epoxy‐9‐octadecenoate, both with double bonds and epoxide groups predominantly ofcis configuration; (c) 13‐oxo‐9,11‐and 9‐oxo‐10, 12‐octadecadienoates; (d) 13‐hydroxy‐9, 11‐ and 9‐hydroxy‐10, 12‐octadecadienoates; (e) 9, 10, 13‐trihydroxy‐11‐ and 9,12,13‐trihydroxy‐10‐octadecenoates. In addition, trace amounts of (f) 11‐hydroxy‐9,10‐epoxy‐12‐and 11‐hydroxy‐12,13‐epoxy‐9‐octadecenoates; (g) 13‐oxo‐9‐hydroxy‐10‐and 9‐oxo‐13‐hydroxy‐11‐octadecenoates; (h) 9,10‐dihydroxy‐12‐ and 12, 13‐dihydroxy‐9‐octadecenoates; and (i) 9,12,13‐dihydroxyethoxy‐10‐ and 9,10,13‐dihydroxyethoxy‐11‐octadecenoates were indicated by mass spectrometry. Dihydroxyethoxy compounds (i) were possibly formed upon extraction of the SPC from flakes by 80% ethanol. Except for the first two epoxy compounds, labelled a and b, the oxygenated fatty acids are similar to the products formed by homolytic decomposition of linoleic acid hydroperoxide. The first two compounds with predominantlycis configuration may occur by action of fatty acid hydroperoxides on an unsaturated fatty acid.

Singlet oxygen formation during hemoprotein catalyzed lipid peroxide decomposition

The singlet oxygen trap diphenylfuran was rapidly oxidized to cis dibenzoylethylene during the decomposition of linoleic acid hydroperoxide catalyzed by ceric ions, methemoglobin or hematin. This conversion was enhanced in a deuterated medium and inhibited by other singlet oxygen quenchers or traps. The chemiluminescence accompanying the decomposition of the linoleic acid hydroperoxide was also markedly enhanced in a deuterated medium and inhibited by other singlet oxygen quenchers or traps. Antioxidants markedly inhibited these reactions. It is concluded that singlet oxygen is formed in substantial quantities during the metal catalyzed decomposition of linoleic acid hydroperoxide.

Homolytic decomposition of linoleic acid hydroperoxide: Identification of fatty acid products

AbstractAn isomeric mixture of linoleic acid hydroperoxides, 13‐hydroperoxy‐cis‐9,trans‐11‐octadecadienoic acid (79%) and 9‐hydroperoxy‐cis‐12,trans‐10‐octadecadienoic acid (21%), was decomposed homolytically by Fe(II) in an ethanol‐water solution. In one series of experiments, the hydroperoxides were decomposed by catalytic concentrations of Fe(II). The 10−5 M Fe(III) used to initiate the decomposition was kept reduced as Fe(II) by a high concentration of cysteine added to the reaction in molar excess of the hydroperoxides. Nine different monomeric (no detectable dimeric) fatty acids were identified from the reaction. Analyses of these fatty acids revealed that they were mixtures of positional isomers identified as follows: (I) 13‐oxo‐trans,trans‐(andcis,trans‐) 9,11‐octadecadienoic and 9‐oxo‐trans,trans‐ (andcis,trans‐) 10,12‐octadecadienoic acids; (II) 13‐oxo‐trans‐9,10‐epoxy‐trans‐11‐octadecenoic and 9‐oxo‐trans‐12, 13‐epoxy‐trans‐10‐octadecenoic acids; (III) 13‐oxo‐cis‐9,10‐epoxy‐trans‐11‐octadecenoic and 9‐oxo‐cis‐12, 13‐epoxy‐trans‐10‐octadecenoic acids; (IV) 13‐hydroxy‐9,11‐octadecadienoic and 9‐hydroxy‐10,12‐octadecadienoic acids; (V) 11‐hydroxy‐trans‐12, 13‐epoxy‐cis‐9‐octadecenoic and 11‐hydroxy‐trans‐9, 10‐epoxy‐cis‐12‐octadecenoic acids; (VI) 11‐hydroxy‐trans‐12, 13‐epoxy‐trans‐9‐octadecenoic and 11‐hydroxy‐trans‐9,10‐epoxy‐trans‐12‐octadecenoic acids; (VII) 13‐oxo‐9‐hydroxy‐trans‐10‐octadecenoic acids; (VIII) isomeric mixtures of 9, 12, 13‐dihydroxyethoxy‐trans‐10‐octadecenoic and 9, 10, 13‐dihydroxyethoxy‐trans‐11‐octadecenoic acids; and (IX) 9, 12, 13‐trihydroxy‐trans‐10‐octadecenoic and 9, 10, 13‐trihydroxy‐trans‐11‐octadecenoic acids. In another experiment, equimolar amounts of Fe(II) and hydroperoxide were reacted in the absence of cysteine. A large proportion of dimeric fatty acids and a smaller amount of monomeric fatty acids resulted. The monomeric fatty acids were examined by gas liquid chromatography‐mass spectroscopy. Spectra indicated that the monomers were largely similar to those produced by the Fe(III)‐cysteine reaction.

Intracellular mechanisms for the decomposition of a lipid peroxide. II. Decomposition of a lipid peroxide by subcellular fractions.

The properties of subcellular fractions of rat liver in catalyzing the decomposition of linoleic acid hydroperoxide have been compared with those of transition salts, heme compounds, and nucleophiles. The properties compared included the range of products produced, the pH dependence of the reaction, and the effects of metal-complexing agents, inhibitors, and hydrogen donors. It was concluded that the decomposition of the hydroperoxide in the liver cell was due principally to reaction with the intracellular nucleophile glutathione by a mechanism catalyzed by the enzyme glutathione peroxidase. In the absence of glutathione, however, both the mitochondrial and microsomal fractions decomposed the hydroperoxide presumably by a radical mechanism probably involving the cytochromes.