Methyl Linoleate Hydroperoxides Research Articles

Chemical Changes of Hydroperoxy-, Epoxy-, Keto- and Hydroxy-Model Lipids under Simulated Gastric Conditions.

Chemical changes occurring in dietary lipid oxidation compounds throughout the gastrointestinal tract are practically unknown. The first site for potential chemical modifications is the stomach due to the strong acidic conditions. In this study, model lipids representative of the most abundant groups of dietary oxidation compounds were subjected to in vitro gastric conditions. Thus, methyl linoleate hydroperoxides were used as representative of the major oxidation compounds formed in food storage at low and moderate temperatures. Methyl 9,10-epoxystearate, 12-oxostearate and 12-hydroxystearate were selected as model compounds bearing the oxygenated functional groups predominantly found in oxidation compounds formed at the high temperatures of frying. Analyses were performed using gas-liquid chromatography/flame ionization detection/mass spectrometry and high performance-liquid chromatography/ultraviolet detection. Losses of methyl 9,10-epoxystearate and linoleate hydroperoxides in the ranges 17.8–58.8% and 42.3–61.7% were found, respectively, whereas methyl 12-oxostearate and methyl 12-hydroxystearate remained unaltered. Although quantitative data of the compounds formed after digestion were not obtained, methyl 9,10-dihydroxystearate was detected after digestion of methyl 9,10-epoxystearate, and some major volatiles were detected after digestion of linoleate hydroperoxides. Overall, the results showed that significant modifications of dietary oxidized lipids occurred during gastric digestion and supported that the low pH of the gastric fluid played an important role.

Endogenous Labile Iron Pool-Mediated Free Radical Generation for Cancer Chemodynamic Therapy

Current chemodynamic therapy (CDT) primarily relies on the delivery of transition metal ions with Fenton activity to trigger hydroxyl radical production from hydrogen peroxide. However, administration of an excess amount of exogenous Fenton-type heavy metals may cause potential adverse effects to human health, including acute and chronic damages. Here, we present a new CDT strategy that uses intracellular labile iron pool (LIP) as the endogenous source of Fenton-reactive metals for eliciting free radical generation, and the discovery of hydroperoxides (R'OOH) as an optimal LIP-mediated chemodynamic agent against cancer. By simulating the metabolic fates of peroxo compounds within cells, R'OOH was found to have excellent free radical-producing ability in the presence of labile iron(II) and to suffer only moderate elimination by glutathione/glutathione peroxidase, which contributes to its superior chemodynamic efficacy. The LIP-initiated nontoxic-to-toxic transition of R'OOH, together with increased LIP levels in tumor cells, enabled efficient and specific CDT of cancer. Moreover, pH/labile iron(II) cascade-responsive nanomedicines comprising encapsulated methyl linoleate hydroperoxide and LIP-increasing agent in pH-sensitive polymer particles were fabricated to realize enhanced CDT. This work not only paves the way to using endogenous Fenton-type metals for cancer therapy but also offers a paradigm for the exploration of high-performance chemodynamic agents activated by intracellular LIP.

Oxidative drying properties of a helmet pentadentate phthalocyanine-derived iron(III) complex

The structure of a hexaisoindoline iron(III) complex reported in 1962 was corrected as the one of a recently described helmet phthalocyanine-like iron(III) complex. Accordingly, its catalytic activities were compared to commercial Co(II) and Fe(II) driers towards the oxidation of bulk FAMEs through oxygen uptake measurements and by ATR-FTIR spectroscopy, as well as its ability to decompose methyl linoleate hydroperoxides. It is shown that the phthalocyanine-like iron(III) complex presents higher catalytic performances at low concentrations and under mild conditions of temperature and pressure, both on the overall oxidation process and on the decomposition steps of the drying chemical process. The efficiency of the phthalocyanine-derived iron(III) complex was confirmed by the drying of an alkyd resin emulsion and a satin white paint formulation which exhibits a very good hardness and a low yellowing of the film.

Iron‐Catalyzed Reaction of γ‐Tocopherol with Methyl Linoleate Hydroperoxides in Solutions

Abstractγ‐Tocopherol is one of the main constituents in vegetable oils and acts as an antioxidant by trapping lipid‐peroxyl radicals. This study reports reaction products of γ‐tocopherol with lipid‐peroxyl radicals formed by iron‐catalyzed decomposition of methyl linoleate hydroperoxides (MeLOOH) in toluene and methanol solutions. The products in toluene solution were tocored, methyl (8a‐dioxy‐γ‐tocopherone)‐epoxyoctadecenoates (γT‐OO‐epoxyMeL), methyl (8a‐dioxy‐γ‐tocopherone)‐octadecadienoates (γT‐OO‐MeL), γ‐tocopherol biphenyl dimer (γTBD), γ‐tocopherol diphenylether dimer (γTED), and adducts of γ‐tocopherol dimers with the MeLOOH‐derived peroxyl radicals (γTED‐OO‐epoxyMeL, γTBD‐OO‐MeL, and γTED‐OO‐MeL). The iron‐catalyzed reaction in toluene proceeded slowly, whereas the reaction in methanol was relatively fast. The reaction products in methanol were γT‐OO‐epoxyMeL and γTED‐OO‐epoxyMeL together with tocored, γTBD, and γTED. The results indicate that the iron‐catalyzed decomposition of MeLOOH in toluene produces both epoxyperoxyl and peroxyl radicals and that the decomposition in methanol yields only the epoxyperoxyl radicals. These peroxyl radicals could react with the 8a‐carbon‐centered radical of γ‐tocopherol or its dimers.

Catalytic activity of primary and secondary driers towards the oxidation and hydroperoxide decomposition steps for the chemical drying of alkyd resin

Abstract The autoxidation of fatty acid methyl esters (FAMEs) derived from colza, sunflower, linseed and tung oils and the oxidation of sunflower FAMEs in the presence of several commercial driers based on Co(II), Mn(II), Fe(II), V(IV), Sr(II), Zr(IV), Ca(II), Zn(II) have been investigated. The oxidation step was studied through oxygen uptake measurements with an automatic O 2 pressure recorder (RapidOxy ® ) and by ATR-FTIR spectroscopy. Pure methyl linoleate hydroperoxides (ROOH) were prepared by photooxidation to follow their decomposition by HPLC in the presence of the driers. Only Co(II), Mn(II) and Fe(II) as primary driers have catalytic effects both on the oxidation and on the ROOH decomposition steps. However, the Co-based drier shows the higher oxidation rate while the Fe-based drier has the greater ROOH decomposition rate. On the other hand, oxidation runs faster by increasing the amount of driers from 2.5 to 25–50 mM but an antioxidant behavior is observed at higher levels. Secondary driers show poor or no catalytic activities both on the oxidation and the ROOH decomposition steps with a conversion ranging from 5 to 9% over 24 h. Combinations of driers were finally investigated to highlight possible synergistic or antagonist effects during the oxidation and hydroperoxides decomposition steps. Synergistic effects were found only on the oxidation stage with Co(II)-Zn(II), Mn(II)-Zn(II) and Fe(II)-Ca(II), while these latter do not have influence on the decomposition step.

Inhibition of Hydroperoxy‐, Keto‐ and Hydroxy‐FAME by Alpha‐ and Delta‐Tocopherol at Rancimat Conditions

AbstractThe effects of α‐ and δ‐tocopherol on inhibition of hydroperoxides, keto and hydroxy compounds under Rancimat conditions, i.e. 100 °C and air bubbling, were studied in samples of fatty acid methyl esters (FAME) obtained from high linoleic (HL) and high oleic (HO) sunflower oils. Primary hydroperoxides from methyl linoleate and methyl oleate and secondary keto and hydroxy compounds derived from methyl linoleate hydroperoxides were analyzed by HPLC–UV‐ELS. Different tocopherol concentrations, namely, 10, 50, 100, 500 and 1000 mg/kg, were tested. Irrespective of the lipid substrate and the initial concentration of tocopherol, results showed that the content of hydroperoxides accumulated during the induction period was remarkably higher in the samples containing δ‐tocopherol. The relative concentrations of oleate hydroperoxides in the HO samples were also higher in the presence of δ‐tocopherol. α‐Tocopherol was more effective in inhibiting hydroperoxides at low levels, with 100 mg/kg as optimal concentration, while δ‐tocopherol displayed optimal protection at 1000 mg/kg. Under the oxidation conditions applied, neither α‐ nor δ‐tocopherol showed a protective effect on hydroperoxide decomposition at any level assayed. Formation of keto‐ and hydroxy‐dienes was more related to the concentration of their hydroperoxide precursors. Furthermore, both tocopherols gave rise to increased concentrations of ketodienes at 500 and 1000 mg/kg compared to the controls. Such an effect was more pronounced for α‐tocopherol and in the HL samples.

The Antioxidative Effect of Fullerenes during the Peroxidation of Methyl Linoleate in Toluene

The antioxidative effect of fullerenes C(60) and C(70) was examined by measuring the inhibition of methyl linoleate (MeL) peroxidation in toluene initiated by 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). The fullerenes retarded the formation of MeL hydroperoxides and lowered the rate of propagation. The reaction rates of fullerenes with AMVN-derived peroxyl radicals were much higher than that of MeL. These results indicate that fullerenes can act as retarders of lipid peroxidation, though their activity is low compared with that of α-tocopherol.

Novel Fluorescent Probe for Analysis of Hydroperoxides Based on Boron Dipyrromethane Fluorophore

A new reagent, N-[2-(diphenylphosphino)ethyl]-4-(1,3,5,7-tetramethyl-4,4-difluoro-4-bora-3a,4a-diaza-s-indacene-8-yl)benzamide (DPPEA-BODIPY), was designed and synthesized for analysis of hydroperoxides. DPPEA-BODIPY fluoresces at low levels in the visible range (lambda(ex)/lambda(em) = 502 nm/515 nm) and reacts with hydroperoxides to produce DPPEA-BODIPY oxide, which fluoresces at high levels. The fluorescence intensity of the reaction mixture was observed to be linearly related to the methyl linoleate hydroperoxide (MeLOOH) concentration.

Photoirradiation of representative polycyclic aromatic hydrocarbons and twelve isomeric methylbenz[a]anthracene with UVA light: formation of lipid peroxidation

Polycyclic aromatic hydrocarbons (PAHs) are widespread genotoxic environmental pollutants, which require metabolic activation in order to exert biological activities, including mutagenicity and carcinogenicity. Photoactivation is another activation pathway that can lead to PAH genotoxicity. In this paper, we demonstrate that photoirradiation of a series of representative PAHs, with and without bearing a methyl substituent, with UVA light in the presence of methyl linoleate resulted in the formation of methyl linoleate hydroperoxides (a lipid peroxide). The lipid peroxide formation was inhibited by dithiothreitol (DTT) (free radical scavenger), NaN3 (singlet oxygen and free radical scavenger), and superoxide dismutase (SOD) (superoxide scavenger), but was enhanced by the presence of deuterium oxide (D2O) (extends singlet oxygen lifetime). These results suggest that photoirradiation of PAHs by UVA light generates reactive oxygen species (ROS), which induce lipid peroxidation.

Photodecomposition of Retinyl Palmitate in Ethanol by UVA LightFormation of Photodecomposition Products, Reactive Oxygen Species, and Lipid Peroxides

Photodecomposition of retinyl palmitate (RP), an ester and the storage form of vitamin A (retinol), in ethanol under UVA light irradiation was studied. The resulting photodecomposition products were separated by reversed-phase HPLC and identified by spectral analysis and comparison with the chromatographic and spectral properties of synthetically prepared standards. The identified products include 5,6-epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, 13-ethoxy-14-hydroxy-RP, anhydroretinol (AR), palmitic acid, ethyl palmitate, and four tentatively assigned cis and trans isomeric 15-ethoxy-ARs. AR was formed as a mixture of all-trans-AR, 6Z-cis-AR, 8Z-cis-AR, and 12Z-cis-AR with all-trans-AR predominating. 5,6-Epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, and 13-ethoxy-14-hydroxy-RP were also formed from reaction of RP with alkylperoxy radicals generated by thermal decomposition of 2,2'-azobis(2,4-dimethylvaleronitrile). Formation of these photodecomposition products was inhibited in the presence of sodium azide (NaN3), a free radical inhibitor. These results suggest that formation of 5,6-epoxy-RP, 4-keto-RP, 11-ethoxy-12-hydroxy-RP, and 13-ethoxy-14-hydroxy-RP from photoirradiation of RP is mediated by a light-initiated free radical chain reaction. AR and the isomeric 11-ethoxy-ARs were not formed from reaction of RP with alkylperoxy radicals generated from 2,2'-azobis(2,4-dimethylvaleronitrile), and their formation was not inhibited when NaN3 was present during the photoirradiation of RP. We propose that these products were formed through an ionic photodissociation mechanism, which is similar to the reported formation of AR through ionic photodissociation of retinyl acetate. RP and all its identified photodecomposition products described above (i) were not mutagenic in Salmonella typhimurium tester strains TA98, TA100, TA102, and TA104 in the presence and absence of S9 activation enzymes, (ii) were not photomutagenic in Salmonella typhimurium TA102 upon UVA irradiation, and (iii) did not bind with calf thymus DNA in the presence of microsomal metabolizing enzymes. These results suggest that RP and its decomposition products are not genotoxic; however, photoirradiation of RP, 5,6-epoxy-RP, and AR with UVA light in the presence of methyl linoleate resulted in lipid peroxide (methyl linoleate hydroperoxides) formation. The lipid peroxide formation was inhibited by dithiothreitol (DTT) (free radical scavenger), NaN3 (singlet oxygen and free radical scavenger), and superoxide dismutase (SOD) (superoxide scavenger) but was enhanced by the presence of deuterium oxide (D2O) (enhancement of singlet oxygen lifetime). These results suggest that photoirradiation of RP, 5,6-epoxy-RP, and AR by UVA light generated reactive oxygen species resulting in lipid (methyl linoleate) peroxidation.

A novel method of following oxidation of low-density lipoprotein using a sensitive fluorescent probe, diphenyl-1-pyrenylphosphine.

Diphenyl-1-pyrenylphosphine (DPPP), which reacts with lipid hydroperoxide stoichiometrically to yield a fluorescent product DPPP oxide (DPPP=O) and the corresponding hydroxide, was used as a fluorescent probe for lipid peroxidation in low-density lipoprotein (LDL). DPPP was successfully incorporated into LDL using the dispersion reagent Pluronic F-127. Incorporation of DPPP into LDL was confirmed by gel filtration chromatography. Reaction of DPPP with hydroperoxide within an LDL particle was examined by monitoring the increase in fluorescence intensity of the LDL. It was found that lipid-soluble hydroperoxides such as methyl linoleate hydroperoxide preferably reacted with DPPP, whereas hydrogen peroxide did not. Fluorescence was increased at the early stages in the oxidation of DPPP-labeled LDL by an azo radical initiator or human neutrophils. LDL, which was labeled with DPPP or DPPP=O, was taken up by cells such as THP-1-derived macrophages and human umbilical vein endothelial cells. The fluorescence of DPPP=O could be observed in cells using fluorescence microscopy equipped with a cooled charge coupled device camera in a nondestructive manner. The present study shows that DPPP is a sensitive, selective, and quantitative probe for monitoring LDL oxidation and visualizing intracellular oxidation.

Methyl linoleate oxidation in the presence of bovine serum albumin.

The oxidation of methyl linoleate (LMe) in the presence of bovine serum albumin (BSA) was studied to analyze both the processes involved when lipid oxidation occurs in the presence of proteins and the relative progression of the several reactions implicated. The disappearance of LMe, the formation of primary and secondary lipid oxidation products, the loss of essential amino acids, and the production of oxidized lipid/amino acid reaction products (OLAARPs) were studied as a function of incubation time. During the first steps of lipid oxidation, LMe was converted quantitatively to methyl linoleate hydroperoxides, which were very rapidly degraded to either secondary products of lipid oxidation or OLAARPs. No significant differences were identified in the major lipid oxidation products formed in incubations with or without proteins, indicating that mechanisms for formation of these compounds are similar in both cases. In addition, no significant differences were observed between the time-courses of formation of secondary oxidation products and OLAARPs, suggesting that hydroperoxide decomposition and OLAARP formation occur simultaneously when the lipid oxidation process takes place in the presence of proteins. Furthermore, OLAARP formation seems to be an unavoidable process that should be considered as a last step in the lipid peroxidation process.

Action of 1-(11-selenadodecyl)-glycerol and 1-(11-selenadodecyl)-3-trolox-glycerol against lipid peroxidation.

The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)-glycerol (SeG) and 1-(11-selenadodecyl)-3-Trolox-glycerol (SeTrG, where Trolox = 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated. We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation, induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution, micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals. SeG reduced methyl linoleate hydroperoxides in organic solution and in methyl linoleate micelles oxidized by ferrous ion (Fe2+)/ascorbic acid. In rat plasma SeG and SeTrG decreased the formation of lipid hydroperoxides generated by hydrophilic azo compounds. SeG and SeTrG spared alpha-tocopherol (alpha-TOH) consumption in multilamellar vesicle membranes oxidized by hydrophilic or lipophilic initiators, and only SeTrG spared alpha-TOH in superoxide/nitric oxide oxidized membranes. In rat plasma oxidized by radical initiators (either hydrophilic or lipophilic) or superoxide/nitric oxide, SeTrG suppressed alpha-TOH consumption, but SeG had no effect. The two selenium-containing compounds showed inhibitory effects on lipid peroxidation that depended on their structure, the medium where they acted, and the oxidant used.

Formation of Active Oxygen Species and Lipid Peroxidation Induced by Hypochlorite

Hypochlorite or its acid, hypochlorous acid, may exert both beneficial and toxic effects in vivo. In order to understand the role and action of hypochlorite, the formation of active oxygen species and its kinetics were studied in the reactions of hypochlorite with peroxides and amino acids. It was found that tert-butyl hydroperoxide and methyl linoleate hydroperoxide reacted with hypochlorite to give peroxyl and/or alkoxyl radicals with little formation of singlet oxygen in contrast to hydrogen peroxide, which gave singlet oxygen exclusively. Amino acids and ascorbate reacted with hypochlorite much faster than peroxides. Free radical-mediated lipid peroxidation of micelles and membranes in aqueous suspensions was induced by hypochlorite, the chain initiation being the decomposition of hydroperoxides by hypochlorite. It was suppressed efficiently by ebselen which reduced hydroperoxides and by α-tocopherol, which broke chain propagation, but less effectively by hydrophilic antioxidants present in the aqueous phase. Cysteine suppressed the oxidation, but it was poorer antioxidant than α-tocopherol. Ascorbate also exerted moderate antioxidant capacity, but it acted as a synergist with α-tocopherol. Taken together, it was suggested that the primary target of hypochlorite must be sulfhydryl and amino groups in proteins and that the lipid peroxidation may proceed as the secondary reaction, which is induced by radicals generated from sulfenyl chlorides and chloramines.

Ascorbic acid and ascorbyl palmitate have only minor effect on the formation and decomposition of methyl linoleate hydroperoxides

Effects of ascorbic acid (AA) and ascorbyl palmitate (AP) on lipid hydroperoxides were evaluated during the formation and decomposition of methyl linoleate hydroperoxides (ML-OOH). AA and AP at 1 and 10 mM levels had no effect on the formation of ML-OOH during the autoxidation of methyl linoleate at 40 °C. However, depending on the reaction medium, AA and AP at 0.2 and 2 mM either slightly inhibited or accelerated the decomposition of 40 mM cis, trans ML-OOH in hexadecane or in hexadecane-inwater emulsion. The increased decomposition rate of ML-OOH, when compared to a control sample, was apparently due to the reductive activity of AA and AP on metal ions present in the system, as the addition of EDTA improved the stability of ML-OOH. The more detailed analysis of the decomposition reactions of ML-OOH suggests that under favorable reaction conditions AA and AP were, to some extent, capable of acting as hydrogen atom donors to peroxyl radicals and reducers of hydroperoxides to more stable hydroxy compounds. However, since all these effects of AA and AP on lipid hydroperoxides were relatively small, it is assumed that the antioxidative activity of AA and AP as well as their effect on the stability and reactions of lipid hydroperoxides in biological systems and in foods is mainly related to their synergistic interactions with other antioxidative compounds such as tocopherols.

Ascorbic acid and ascorbyl palmitate have only minor effect on the formation and decomposition of methyl linoleate hydroperoxides

Effects of ascorbic acid (AA) and ascorbyl palmitate (AP) on lipid hydroperoxides were evaluated during the formation and decomposition of methyl linoleate hydroperoxides (ML-OOH). AA and AP at 1 and 10 mM levels had no effect on the formation of ML-OOH during the autoxidation of methyl linoleate at 40 °C. However, depending on the reaction medium, AA and AP at 0.2 and 2 mM either slightly inhibited or accelerated the decomposition of 40 mM cis, trans ML-OOH in hexadecane or in hexadecane-inwater emulsion. The increased decomposition rate of ML-OOH, when compared to a control sample, was apparently due to the reductive activity of AA and AP on metal ions present in the system, as the addition of EDTA improved the stability of ML-OOH. The more detailed analysis of the decomposition reactions of ML-OOH suggests that under favorable reaction conditions AA and AP were, to some extent, capable of acting as hydrogen atom donors to peroxyl radicals and reducers of hydroperoxides to more stable hydroxy compounds. However, since all these effects of AA and AP on lipid hydroperoxides were relatively small, it is assumed that the antioxidative activity of AA and AP as well as their effect on the stability and reactions of lipid hydroperoxides in biological systems and in foods is mainly related to their synergistic interactions with other antioxidative compounds such as tocopherols.

Estimation of lipid peroxidation of live cells using a fluorescent probe, Diphenyl-1-pyrenylphosphine

Diphenyl-1-pyrenylphosphine (DPPP), which reacts with lipid hydroperoxides stoichiometrically to yield fluorescent product DPPP oxide, was used as a fluorescent probe for lipid peroxidation in live cells. DPPP was successfully incorporated into U937 cells. Incorporation of DPPP into the cell membrane was confirmed by fluorescence microscopy. Reaction of DPPP with hydroperoxides was examined by monitoring increase in fluorescence intensity of the cell. It was found that lipid-soluble hydroperoxides such as methyl linoleate hydroperoxide preferably react with DPPP, whereas hydrogen peroxide did not react with DPPP located in the membrane. Linear correlation between increase in fluorescence intensity and the amount of methyl linoleate hydroperoxide applied to the cell was observed. DPPP gave little effect on cell proliferation, cell viability or cell morphology for at least 3 d. DPPP oxide, fluorescent product of DPPP, was quite stable in the membrane of living cells for at least 2 d. Fluorescence of DPPP-labeled cells was measured after treating with diethylmaleate (DEM), or 2,2′-Azobis(2-amidinopropane) dihydrochloride (AAPH), or culturing with low serum content. These reagents and culture condition induced dose- and/or time-dependent increase in fluorescence. Addition of vitamin E effectively suppressed increase in fluorescence. When DPPP-labeled cells and DCFH-DA-labeled cells were treated with NO, H 2O 2, AAPH, and DEM to compare the formation of hydoperoxides in the membrane and cytosol, distinct patterns of peroxide formation were observed. These results indicate that fluorescent probe DPPP is eligible for estimation of lipid peroxidation proceeding in the membrane of live cells, and use of this probe is especially advantageous in long-term peroxidation of the cell.

α-, γ- and δ- Tocopherols as inhibitors of isomerization and decomposition of cis,trans methyl linoleate hydroperoxides

α-, γ- and δ- Tocopherols as inhibitors of isomerization and decomposition of cis,trans methyl linoleate hydroperoxides

α-, γ- and δ- Tocopherols as inhibitors of isomerization and decomposition ofcis,trans methyl linoleate hydroperoxides

The effects of α-, γ- and δ-tocopherols on the stability and decomposition reactions of lipid hydroperoxides were studied. Isomerization and decomposition of cis,trans methyl linoleate hydroperoxides (cis,trans ML-OOH) in hexadecane at 40 °C were followed by high-performance liquid chromatography. Due to its higher hydrogen donating ability, α-tocopherol was more efficient than γ- and δ-tocopherols in inhibiting the isomerization of cis,trans ML-OOH to trans,trans ML-OOH. α-Tocopherol stabilized hydroperoxides into the cis,trans configuration, whereas γ- and δ-tocopherols allowed hydroperoxides to convert into trans,trans isomers. Thus, the biological importance of α-tocopherol as compared to other tocopherols may be partly due to its better efficacy in protecting the cis,trans configuration of hydroperoxides formed, for example, in the enzymatic oxidation of polyunsaturated fatty acids. The isomeric configuration of hydroperoxides has an impact on biological activities of further oxidation products of polyunsaturated fatty acids. Paradoxically, the order of activity of tocopherols with regard to hydroperoxide decomposition was different from that obtained for hydroperoxide isomerization. γ- and δ-tocopherols were more efficient inhibitors of ML-OOH decomposition when compared to α-tocopherol. A loss of antioxidant efficiency, observed as the tocopherol concentration increased from 2 to 20 mM, was highest for α-tocopherol but was also evident for γ- and δ-tocopherols. Thus, the differences in the relative effects of tocopherols at differing concentrations seem to result from a compromise between their radical scavenging efficiency and participation in side reactions of peroxidizing nature.

No effect of esterification with fatty acid on antioxidant activity of lutein

Antioxidant activities of lutein and lutein myristate esters were evaluated by using both the methyl linoleate hydroperoxide method and colorimetry of the quenching activity against 1,1-diphenyl-2-picrylhydrazyl. The antioxidant activities of free lutein (FL), lutein monomyristate ester (LM) and lutein dimyristate ester (LD) were not significantly different in both methods. No synergetic effects among FL, LM and LD were obtained. These results suggest that esterification of OH groups with fatty acids might not affect antioxidant activity of lutein.