Methyl Linoleate Hydroperoxides Research Articles

Decomposition products of dimers arising from secondary oxidation of methyl linoleate hydroperoxides.

Dimers formed in aerated methyl linoleate hydroperoxides were decomposed in liquid paraffin by bubbling with dry air at 30°C for 24 hr to identify the decomposition products. The aerated dimers were fractionated according to their molecular weights by gel permeation chromatography. Identification of the monomeric (25.6%) and low molecular fission products (10.8%) by gas chromatography-mass spectrometry showed the major monomers as methyl hydroxy-octadecadienoate, methyl hydroxy (or hydroperoxy)-epoxy-octadecenoate, methyl dihydroxy (or hydroperoxy)-octadecenoate, methyl trihydroxy (or hydroperoxy)-octadecenoate; and the major fission products as methyl 8-hydroxy-octanoate, 4-hydroxy (or hydroperoxy)-nonanal or -2-nonenal, methyl 12-oxo-9-hydroxy (or hydroperoxy)-dodecanoate or -10-dodecenoate, and methyl 11-oxo-9-undecenoate.The monomeric products were presumed to be derived from alkoxy radicals generated by the cleavage of peroxy linkages in the dimers, whereas the low molecular products were suggested t...

Different rates of geometric isomers of linoleate hydroperoxide in acid-catalyzed decomposition.

Methyl linoleate hydroperoxide was decomposed with 0.1 m HCl in acetone-water (9:1, v/v) at 30°C. The decrease in four isomers of the hydroperoxide was monitored by HPLC without any derivatization. In both isomers having 13- and 9-hydroperoxy groups, those having trans, trans dienes decomposed more rapidly than those having cis, trans dienes. In all the isomers, the rates of decomposition were first order with respect to concentrations of the hydroperoxides. The yields of 2-nonenal and 12-oxo-10-dodecenoate were also measured by GC-MS. 12-Oxo-10-dodecenoate was produced only from the 13-isomers and 2-nonenal from the 9-isomers. The rapid decomposition of the trans, trans isomers didn’t seem to be responsible for the formation of these aldehyde products.

A Simple Method for Preparation of Pure Isomers of Methyl Linoleate Hydroperoxide by Dry Silica Gel Column Chromatography

A Simple Method for Preparation of Pure Isomers of Methyl Linoleate Hydroperoxide by Dry Silica Gel Column Chromatography

Oxidation of lipids. XI. Spin trapping and identification of peroxy and alkoxy radicals of methyl linoleate

Spin trapping of peroxy and alkoxy radicals generated from the hydroperoxide of methyl linoleate was studied using methyl- N-duryl nitrone (MDN) and phenyl- N-tert-butyl nitrone (PBN) as spin traps. The conjugated dienyl carbon radical was also generated from methyl linoleate and spin-trapped. The spin adducts of peroxy, alkoxy, and dienyl carbon radicals were observed by ESR and their hyperfine splitting constants were determined. The spin adducts of peroxy and alkoxy radicals could be distinguished clearly with MDN.

Oxidation of Lipids. IX. Decomposition of Methyl Linoleate and Methyl Linolenate Hydroperoxides in Solution

Abstract Decompositions of methyl linoleate hydroperoxide (LOOH) induced by di-t-butyl diperoxyoxalate and cobalt ions were investigated in benzene at 50 °C under vacuum to elucidate the degradation mechanism. The major products were dimer (LOOL), oxodiene, hydroxydiene and epoxyhydroxyene (and/or epoxyoxoene). It was suggested that these products were formed by the recombination of L· and LOO· radicals, β-scission of LO· radical, hydrogen abstraction of LO· radical, and intramolecular epoxidation of LOO· radical, respectively. The decomposition of methyl linolenate hydroperoxide (L′OOH) was also studied. The major products were dimer, oxotriene, hydroxytriene, and thiobarbituric acid reactive substances, which were suggested to be formed by the intramolecular cyclization of L′OO· radical.

Linoleate hydroperoxides are cleaved heterolytically into aldehydes by a Lewis acid in aprotic solvent.

Treatment of isomeric methyl linoleate hydroperoxides with a Lewis acid, BF3, in anhydrous ether led to a carbon-to-oxygen rearrangement that caused cleavage into shorter-chain aldehydes. Methyl (9Z,11E)-13-hydroperoxy-9,11-octadecadienoate afforded mainly hexanal and methyl (E)-12-oxo-10-dodecenoate, whereas methyl (10E,12Z)-9-hydroperoxy-10,12-octadecadienoate cleaved into 2-nonenal and methyl 9-oxononanoate. The 2 aldehydes obtained from each hydroperoxide isomer were uncharacteristic of the complex volatile profile usually obtained by β-scission of oxy radicals derived from homolysis of the hydroperoxide group. Rather, the reaction resembled the one catalyzed by the plant enzyme, hydroperoxide lyase.

Methyl linoleate dimer and methyl 8-phenyloctanoate in the copper-catalyzed decomposition products of methyl linoleate hydroperoxides.

Methyl linoleate dimer and methyl 8-phenyloctanoate in the copper-catalyzed decomposition products of methyl linoleate hydroperoxides.

Importance of oxidative degradation on peroxide-decomposing activities of antarctic krill phospholipids.

The peroxide-decomposing activity of Antarctic krill Euphausia superba lipid was studied. Chromatographic analysis by silicic acid showed that krill phospholipids are mainly composed of phosphatidyl choline (PC) with phosphatidyl ethanolamine, lysoPC and oxygenated polar materials. All chromatographic fractions showed varying activity in the decomposition of methyl linoleate hydroperoxides. In order to elucidate the mechanism of peroxide degradation, the tion, partial hydrolysis and oxidation for different periods of time. With hydrogenation, peroxidedecomposing activity was lost and the browning of PC was inhibited as well, With the progress of oxidation, both the peroxide-decomposing activity and the browning of PC were enhandced. Hydrolysis of any part of PC decreased the peroxide-decomposing activity. These results suggest that oxidative degradation is necessary for phospholipids to show peroxide-decomposing activity.

Properties of thiobarbituric acid-reactive materials obtained from lipid peroxide and tissue homogenate.

In order to classify the 2-thiobarbituric acid (TBA)-reactive materials in various tissues, control and CCl4-intoxicated rat liver homogenates as well as methyl linoleate hydroperoxide (MLHPO) and malonaldehyde were subjected to the TBA reaction under both aerobic and anaerobic conditions. The TBA reaction of malonaldehyde proceeded regardless of the absence of oxygen, while the TBA value obtained from MLHPO catalyzed by tissue under anaerobic conditions was as low as 15% of the aerobic value, and tissue homogenate, even prepared from CCl4-intoxicated rat liver, gave practically no color development under anaerobic conditions. However, after an aerobic preincubation, MLHPO and tissue homogenate produced TBA-reactive materials which could react with TBA even under anaerobic conditions. These TBA-reactive materials are not malonaldehyde itself but seem to be some further-oxidized and more polar lipid hydroperoxide. The addition of Fe to the TBA reaction medium seems to negate the requirement for oxygen. The magnitude of the TBA value obtained anaerobically from tissue with Fe addition was similar to the TBA value obtained aerobically from tissue without Fe addition.

The effect of methyl linoleate hydroperoxide (MLHP), a possible toxic intermediate of ozone, on human normal and glucose‐6‐phosphate dehydrogenase (G‐6‐PD) deficient erythrocytes

Abstract Erythrocytes of both normal and G‐6‐PD deficient humans responded in a dose‐dependent manner to the oxidant stress of MLHP as measured by decreases in G‐6‐PD activity, increases in methemoglobin (METHB) levels and decreases in reduced glutathione (GSH). The G‐6‐PD deficient eryth‐rocytes displayed a markedly enhanced sensitivity to MLPH induced decreases in G‐6‐PD activity and METHB increases while being less sensitive than normal erythrocytes to changes in GSH levels.

Antioxidative effects of .ALPHA.-tocopherol and riboflavin-butyrate in rats dosed with methyl linoleate hydroperoxide.

The antioxidative effects of dietary α-tocopherol (TOC) and riboflavin-tetrabutyrate (RTB) against tissue lipoperoxidation caused by the long-term administration of methyl linoleate hydroperoxide (HPO) to rats were investigated by measuring the spontaneous chemiluminescence (CL) intensities and thiobarbituric acid (TBA) reactants of the liver, lung and heart.TOC supplementation resulted in the effective decrease of CL intensities and TBA reactants in the three organs, while RTB supplementation led to the definitive decay of both indices of the lung and a significant decrease in the CL intensity of the heart, as compared with those of rats dosed with HPO and not given any supplemental antioxidant.Although the activities of glutathione peroxidase and glutathione reductase in the three organs obtained from rats dosed with HPO for 29 days were clearly lower than those of the control rats, both enzyme activities in rats dosed with antioxidants other than HPO were generally maintained at levels almost equal to ...

An evaluation of the dorset sheep as a predictive animal model for the response of G‐6‐PD deficient human erythrocytes to a proposed systemic toxic ozone intermediate, methyl linoleate hydroperoxide

Erythrocytes of both G-6-PD deficient humans and Dorset sheep, an animal model with an erythrocyte G-6-PD deficiency, both responded in a dose dependent manner to the oxidant stress of MOHP as measured by decreases in G-6-PD activity, increases in METHB levels and decreases in GSH. However, the human G-6-PD deficient erythrocytes were considerably more sensitive to the formation of METHB than the sheep erythrocytes while the reverse was the case for the GSH parameter. The results suggest a qualitative difference in the response of sheep erythrocytes and human G-6-PD deficient erythrocytes to MOHP that seriously questions the value of the sheep erythrocyte as a quantitatively accurate predictive model.

Tissue lipid peroxidation and ultraweak chemiluminescence in rats dosed with methyl linoleate hydroperoxide.

This study was undertaken to elucidate the toxic nature of dietary hydroperoxides in rats by the measurement of tissue chemiluminescence (CL). By the oral administration of methyl linoleate hydroperoxide (HPO) for two days, the tissue CL intensities and thiobarbituric acid (TBA) reactants were significantly increased in the liver, kidney, heart and lung, and the increases of both indices were inhibited by the supplemental administration of antioxidants, i.e. d-α-tocopherol (TOC) and riboflavin-tetrabutyrate (RTB). TOC was especially effective on the liver and kidney and RTB was effective on the liver, lung and heart. Hepatic glutathione peroxidase activity was evidently elevated at the seventh day of HPO-feeding, and this activation resulted in the decay of CL intensities and TBA reactants in rat organs. The spectrum of CL from liver homogenates of rats dosed with HPO for two days revealed five emission bands in the visible region and was similar to that for a singlet oxygen.The results indicate that TOC ...

Absorption and Metabolism of Methyl Linoleate Hydroperoxides in Rats

The intestinal absorption of methyl linoleate hydroperoxides (MLHPs) in rats was studied. After oral administration of MLHPs, lymph was collected continuously from the thoracic ducts for 36h. The lipids in the collected lymph were extracted and analyzed by high performance liquid chromatography (HPLC).The resulting data suggest that part of the MLHPs administered was absorbed directly from the intestinal wall and in part converted to some derivatives such as methyl hydroxyoctadecadienoates (MHODs) and methyl oxooctadecadienoates (MOODs) which were also absorbed from the intestinal wall.

Epoxidation of cholesterol by hepatic microsomal lipid hydroperoxides

[1,2-3H]Cholesterol was epoxidized to radioactive cholesterol α- and β-epoxides (5,6α-epoxy-5α- and 5,6β-epoxy-5β-cholestan-3β-ols) in the ratio 1:4 by hepatic microsomal lipid hydroperoxides (MsOOH, 1 mM as active oxygen) in the presence of ferrous ion. MsOOH could be replaced by methyl linoleate hydroperoxides (MOOH) under the same conditions although the latter was less effective than the former. None of cumene hydroperoxide, t-butyl hydroperoxide, and hydrogen peroxide was an effective oxidant even at 10 mM. Neither ADP nor EDTA had an effect on the epoxidation of cholesterol by MsOOH as well as by MOOH. Ferrous ion could not be replaced by ferric ion in the hydroperoxide-mediated epoxidation. Cyanide anion potentially inhibited the reaction.

Formation of dimers during the initial stage of autoxidation in methyl linoleate.

The formation of dimers in the initial stage of methyl linoleate (ML) autoxidation was demonstrated. The oxidation profile of freshly prepared ML was followed by TLC during autoxidation by aeration at 30°C for 192 hr. After 24 hr of autoxidation, the peroxide value of ML was still 0.6, and two unknown polar spots appeared besides intact ML and methyl linoleate hydroperoxides (MLHPO). These two spots were identified as dimers by successive gel and high performance liquid chromatographic separations and by molecular weight determination. The ratio of dimers/MLHPO reached a maximum (0.74) after 96 hr of autoxidation. This result indicates that the formation of dimers in the initial stage of autoxidation was slightly less than that of MLHPO. The dimers were linked through -C-O-O-C- bonds and contained hydroperoxy and/or carbonyl groups and conjugated dienes.

脂質ハイドロパーオキサイドのチオバルビツール酸(TBA)反応における分解触媒の役割

The thiobarbituric acid (TBA) method of lipid hydroperoxide requires Fe catalyst to decompose the hydroperoxide to TBA-reactive secondary products during the reaction. In order to characterize the role of Fe catalyst, FeCl3, ferritin, hemin, defatted tissue homogenate and whole tissue homogenate, were employed for the reaction of methyl linoleate hydroperoxide (MLHPO) with TBA. The results are as follows : 1) Non-heme iron (FeCl3, ferritin) could play as an effective catalyst at a wide range of concentration, while hemin in high concentration suppressed the color intensity of optimum condition. The maximum efficiency of Fe catalyst existing in tissue homogenate lies between non-heme iron and hemin. 2) The TBA reaction catalyzed by FeCl3 or ferritin was inhibited by EDTA, but not by BHT. The reverse effect of BHT and EDTA was observed in hemin or tissue homogenate catalysts. 3) The TBA reaction catalyzed with fresh FeCl3 proceeded regardless the absence of oxygen, while the TBA value obtained with aged FeCl3, ferritin, hemin or tissue homogenate was significantly depressed under anaerobic conditions. 4) The catalytic activity in rat liver tissue was distributed similarly among all subcellular fractions, but 105000×g pellet showed the highest effect per unit of protein.

Effect of Some Fatty Acid Methyl Esters on Gastrointestinal Carcinogenesis by <italic>N</italic>-Methyl-<italic>N</italic>′-nitro-<italic>N</italic>-nitrosoguanidine in Rats<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

Methyl linoleate hydroperoxide (MLHP) and native methyl linoleate (ML) were tested for carcinogenicity toward the gastrointestinal (GI) tract in male specific-pathogen-free outbred Wistar rats. N-Methyl-N-nitro-N-nitrosoguanidine (MNNG) was given in the drinking water in a dose of 20 mg/liter when cocarcinogenic properties of the test substances were to be tested. MLHP and ML were fed by stomach tube and had no effect as complete carcinogens. Given concomitantly with MNNG, ML did not enhance carcinogenesis. MLHP in conjunction with MNNG was the only treatment which, as treatment with MNNG in a dose of 83 mg/liter, led to an increase of GI cancers in animals that died before day 354. Cumulative results after a maximum of 612 days showed a distribution of GI cancers in favor of the glandular stomach only after MLHP was given with MNNG.

Differential effects of methyl linoleate hydroperoxides on respiratory activities of rat heart mitochondria

Differential effects of methyl linoleate hydroperoxides on respiratory activities of rat heart mitochondria

うさぎにおけるリノール酸メチルヒドロペルオキシドの吸収について

The absorption of methyl linoleate hydroperoxides (MLHPs) in rabbit was investigated. After oral administration of 700 mg of MLHPs, lymph was collected continuously from the thoracic duct for 2.5 h. The lipids in the collected lymph were extracted and analyzed by high performance liquid chromatography.The data showed that 0.23% of the dosed MLHPs were contained in the lymph as intact MLHPs. This result indicates that some unchanged hydroperoxides are absorbed into intestinal wall and transported to some organs through lymph.