Autoxidation Products Research Articles

Autoxidation Products of the Methanolic Extract of the Leaves of Combretum micranthum Exert Antiviral Activity against Tomato Brown Rugose Fruit Virus (ToBRFV).

Tomato brown rugose fruit virus (ToBRFV) is a new damaging plant virus of great interest from both an economical and research point of view. ToBRFV is transmitted by contact, remains infective for months, and to-date, no resistant cultivars have been developed. Due to the relevance of this virus, new effective, sustainable, and operator-safe antiviral agents are needed. Thus, 4-hydroxybenzoic acid was identified as the main product of the alkaline autoxidation at high temperature of the methanolic extract of the leaves of C. micranthum, known for antiviral activity. The autoxidized extract and 4-hydroxybenzoic acid were assayed in in vitro experiments, in combination with a mechanical inoculation test of tomato plants. Catechinic acid, a common product of rearrangement of catechins in hot alkaline solution, was also tested. Degradation of the viral particles, evidenced by the absence of detectable ToBRFV RNA and the loss of virus infectivity, as a possible consequence of disassembly of the virus coat protein (CP), were shown. Homology modeling was then applied to prepare the protein model of ToBRFV CP, and its structure was optimized. Molecular docking simulation showed the interactions of the two compounds, with the amino acid residues responsible for CP-CP interactions. Catechinic acid showed the best binding energy value in comparison with ribavirin, an anti-tobamovirus agent.

Products of Prolonged Autoxidation of Simple Dihydric Phenols in the Presence of Copper(II) Ions – An Electron Spin Resonance Study

Electron spin resonance (ESR) spectroscopy was used for characterizing the products obtained by prolonged autoxidation of simple dihydric phenols (hydroquinone, catechol, and 4-methylcatechol) in the presence of copper(II) ions. Room temperature ESR spectra revealed that both paramagnetic copper(II) ions and organic radicals are present in obtained autoxidation products similarly to the humic acid complexed copper(II) ions. The ratio of organic radical signal intensity to the copper(II) ion signal intensity suggests that the smallest amount of copper(II) ions is incorporated in the hydroquinone autoxidation product while the highest amount of copper(II) ions is incorporated in the autoxidation product of catechol. Satisfactory computer simulations of experimental ESR spectra were obtained by considering only one type of copper(II) ion binding site for hydroquinone autoxidation product and two distinct types of copper(II) ion binding sites for catechol and 4-methylcatechol autoxidation products. Parameters obtained by the computer simulation of ESR spectra indicated prevalent ionic bonding of copper(II) ions in polymeric matrices with tetrahedral distortion at copper(II) ion binding sites and negligible exchange interactions between them. Products obtained by the hydroquinone and catechol autoxidation have more similar characteristics in comparison to the product obtained by the 4-methylcatechol autoxidation where more expressed ionic bonding of copper(II) ions, and smaller tetrahedral distortion are present. Due to the dipolar interactions of oxygen-centered organic radicals in autoxidation products with paramagnetic copper(II) ions, their ESR linewidths are larger and g-values smaller in comparison to the values found in humic acids from various soil types.

Destruction of polyunsaturated alkyl/acyl and alkenyl/acyl glycerophosphocholine of plasma lipoproteins during incubation with group V and X secretory phospholipase A2s

Plasma lipoproteins are carriers of various glycerophospholipids including diacyl, alkenyl/acyl, and alkyl/acyl glycerophosphocholines (GPCs), which become distributed among cells and tissues during metabolism. For metabolic function, these phospholipids require hydrolysis by phospholipases, but the responsible enzymes have not been identified. We had previously shown that after complete digestion of lipoprotein diacyl- and oxo-diacyl-GPCs, degradation of residual alkyl/acyl and alkenyl/acyl GPCs continues, despite the fact that ether lipids are resistant to hydrolysis by Ca2+ -activated secretory PLA2 s and require the presence of the Ca2+ -independent PLA2 . In the course of further investigation, we came across a report by Khaselev and Murphy in which the autoxidative degradation of plasmalogens in the presence of 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) proceeded beyond the formation of dihydroperoxides, hydroxides and epoxides, and led to an attack on the enyl bond of the plasmalogen, resulting in formation of 1-OH/2-20:4-GPC and 1-formyl/2-20:4-GPC. Our preliminary investigation indicated that lipoprotein 16:0p/20:4ω6-GPC yielded the same autoxidation products as those reported for synthetic 16:0p/20:4ω6-GPC in the presence of AAPH. Such autoxidative degradation of lipoprotein plasmalogens had not been previously reported with or without AAPH. Subsequent study led to the conclusion that this reaction was not limited to arachidonates, but extended to other polyunsaturated eicosanoids, docosanoids, and tetracosanoids, as well as oligounsaturated octadecanoids. These observations led to a hypothesis that the autoxidative cleavage of the lipoprotein plasmalogens proceeded under the influence of apo-protein-derived free radicals as intermediates of oxidative processes.

Monolayer autoxidation of arachidonic acid to epoxyeicosatrienoic acids as a model of their potential formation in cell membranes

In light of the importance of epoxyeicosatrienoic acids (EETs) in mammalian pathophysiology, a nonenzymatic route that might form these monoepoxides in cells is of significant interest. In the late 1970s, a simple system of arranging linoleic acid molecules on a monolayer on silica was devised and shown to yield monoepoxides as the main autoxidation products. Here, we investigated this system with arachidonic acid and characterized the primary products. By the early stages of autoxidation (∼10% conversion of arachidonic acid), the major products detected by LC-MS and HPLC-UV were the 14,15-, 11,12-, and 8,9-EETs, with the 5,6-EET mainly represented as the 5-δ-lactone-6-hydroxyeicosatrienoate as established by 1H-NMR. The EETs were mainly the cis epoxides as expected, with minor trans configuration EETs among the products. 1H-NMR analysis in four deuterated solvents helped clarify the epoxide configurations. EET formation in monolayers involves intermolecular reaction with a fatty acid peroxyl radical, producing the EET and leaving an incipient and more reactive alkoxyl radical, which in turn gives rise to epoxy-hydro(pero)xides and other polar products. The monolayer alignment of fatty acid molecules resembles the arrangements of fatty acids in cell membranes and, under conditions of lipid peroxidation, this intermolecular mechanism might contribute to EET formation in biological membranes.

New degradation mechanism of black tea pigment theaflavin involving condensation with epigallocatechin-3-O-gallate

Theanaphthoquinone (TNQ) is the initial and main oxidation product of theaflavin, a representative black tea pigment. Nevertheless, TNQ is virtually undetected in the high-performance liquid chromatography analysis of black tea leaves using photodiode array detection. To elucidate the degradation mechanism of theaflavin in the black tea production process, this study investigated the reaction of TNQ with epigallocatechin-3-O-gallate (EGCg), which is the most abundant polyphenol in tea leaves. In citrate–phosphate buffer solution at pH 6 and room temperature, TNQ reacted nonenzymatically with EGCg to afford three products, whose structures were determined on the basis of spectroscopic data. The results indicated that the double bond of the ortho-naphthoquinone moiety in TNQ reacted with the autoxidation product of EGCg. This study demonstrates novel reactions occurring in the process of theaflavin degradation, which might be involved in the formation of thearubigins, the major black tea pigments composing oligomeric catechin oxidation products.

Robustness of nitric oxide detoxification to nitrogen starvation in Escherichia coli requires RelA

Reactive nitrogen species and nutrient deprivation are two elements of the immune response used to eliminate pathogens within phagosomes. Concomitantly, pathogenic bacteria have evolved defense systems to cope with phagosomal stressors, which include enzymes that detoxify nitric oxide (•NO) and respond to nutrient scarcity. A deeper understanding of how those defense systems are deployed under adverse conditions that contain key elements of phagosomes will facilitate targeting of those systems for therapeutic purposes. Here we investigated how Escherichia coli detoxifies •NO in the absence of useable nitrogen, because nitrogen availability is limited in phagosomes due to the removal of nitrogenous compounds (e.g., amino acids). We hypothesized that nitrogen starvation would impair •NO detoxification by E. coli because it depresses translation rates and the main E. coli defense enzyme, Hmp, is synthesized in response to •NO. However, we found that E. coli detoxifies •NO at the same rate regardless of whether useable nitrogen was present. We confirmed that the nitrogen in •NO and its autoxidation products could not be used by E. coli under our experimental conditions, and discovered that •NO eliminated differences in carbon and oxygen consumption between nitrogen-replete and nitrogen-starved cultures. Interestingly, E. coli does not consume measurable extracellular nitrogen during •NO stress despite the need to translate defense enzymes. Further, we found that RelA, which responds to uncharged tRNA, was required to observe the robustness of •NO detoxification to nitrogen starvation. These data demonstrate that E. coli is well poised to detoxify •NO in the absence of useable nitrogen and suggest that the stringent response could be a useful target to potentiate the antibacterial activity of •NO.

Isolation and structural elucidation of dimeric epigallocatechin-3-gallate autoxidation products and their antioxidant capacity

Dietary polyphenols like epigallocatechin-3-gallate (EGCG)—which represents the most abundant flavan-3-ol in green tea—are subject of several studies regarding their bioactivity and health-related properties. On many occasions, cell culture or in vitro experiments form the basis of published data. Although the stability of these compounds is observed to be low, many reported effects are directly related to the parent compounds whereas the impact of EGCG degradation and autoxidation products is not yet understood and merely studied. EGCG autoxidation products like its dimers theasinensin A and D, “P2” and oolongtheanin are yet to be characterized in the same extent as their parental polyphenol. However, to investigate the bioactivity of autoxidation products—which would minimize the discrepancy between in vitro and in vivo data—isolation and structure elucidation techniques are urgently needed. In this study, a new protocol to acquire the dimers theasinensin A and D as well as oolongtheanin is depicted, including a variety of spectroscopic and quadrupole time-of-flight high-resolution mass spectrometric (qTOF-HRMS) data to characterize and assign these isolates. Through nuclear magnetic resonance (NMR) spectroscopy, polarimetry, and especially circular dichroism (CD) spectroscopy after enzymatic hydrolysis the complementary atropisomeric stereochemistry of the isolated theasinensins is illuminated and elucidated. Lastly, a direct comparison between the isolated EGCG autoxidation products and the monomer itself is carried out regarding their antioxidant properties featuring Trolox equivalent antioxidant capacity (TEAC) values. These findings help to characterize these products regarding their cellular effects and—which is of special interest in the flavonoid group—their redox properties.

Regulation of hepatic coenzyme Q biosynthesis by dietary omega-3 polyunsaturated fatty acids

Dietary fats are important for human health, yet it is not fully understood how different fats affect various health problems. Although polyunsaturated fatty acids (PUFAs) are generally considered as highly oxidizable, those of the n-3 series can ameliorate the risk of many age-related disorders. Coenzyme Q (CoQ) is both an essential component of the mitochondrial electron transport chain and the only lipid-soluble antioxidant that animal cells can synthesize. Previous work has documented the protective antioxidant properties of CoQ against the autoxidation products of PUFAs. Here, we have explored in vitro and in vivo models to better understand the regulation of CoQ biosynthesis by dietary fats. In mouse liver, PUFAs increased CoQ content, and PUFAs of the n-3 series increased preferentially CoQ10. This response was recapitulated in hepatic cells cultured in the presence of lipid emulsions, where we additionally demonstrated a role for n-3 PUFAs as regulators of CoQ biosynthesis via the upregulation of several COQ proteins and farnesyl pyrophosphate levels. In both models, n-3 PUFAs altered the mitochondrial network without changing the overall mitochondrial mass. Furthermore, in cellular systems, n-3 PUFAs favored the synthesis of CoQ10 over CoQ9, thus altering the ratio between CoQ isoforms through a mechanism that involved downregulation of farnesyl diphosphate synthase activity. This effect was recapitulated by both siRNA silencing and by pharmacological inhibition of farnesyl diphosphate synthase with zoledronic acid. We highlight here the ability of n-3 PUFAs to regulate CoQ biosynthesis, CoQ content, and the ratio between its isoforms, which might be relevant to better understand the health benefits associated with this type of fat. Additionally, we identify for the first time zoledronic acid as a drug that inhibits CoQ biosynthesis, which must be also considered with respect to its biological effects on patients.

Water content, critical micelle concentration of phospholipids and formation of association colloids as factors influencing autoxidation of rapeseed oil.

The exact mechanism of lipid autoxidation in vegetable oils, taking into account physical aspects of this phenomenon, including the role of association colloids, is still not fully understood. The purpose of this study was to consider changes in moisture content and DOPC phospholipid (1,2-dioleoyl-sn-glycero-3-phosphocholine) critical micelle concentration (CMC) in rapeseed oil during autoxidation as well as to find the relationship between these parameters and the accumulation of primary and secondary lipid oxidation products. The experiments were performed at initial oil humidity 220 ppm and 700 ppm, with DOPC below and above CMC. The increase in water concentration was favored by the presence of phospholipids above CMC and, at the same time, high initial water level, which favored oxidation processes and the creation of amphiphilic autoxidation products. At relatively high water level and low amphiphilic DOPC concentration, the growth of water content does not affect the concentration of oxidation products. Amphiphilic substances play a significant role in increasing the water content of oil. Autoxidation products may reduce CMC of DOPC, but water is able to compensate for the CMC-reducing effect of oxidation products. The presence of association colloids and initial water content play a crucial role in the oxidation process of rapeseed oil. The increase in water concentration does not cause a sufficiently large increase in the number of micelles or sufficiently significant changes in their structure to effect an increase in the level of oxidation products. The formation of micelles requires an appropriate content of both water and amphiphilic substances derived from seeds (phospholipids). © 2021 Society of Chemical Industry.

Development of a Detailed Kinetic Model for the Oxidation of n-Butane in the Liquid Phase.

The chemistry underlying liquid-phase oxidation of organic compounds, the main cause of their aging, is characterized by a free-radical chain reaction mechanism. The rigorous simulation of these phenomena requires the use of detailed kinetic models that contain thousands of species and reactions. The development of such models for the liquid phase remains a challenge as solvent-dependent thermokinetic parameters have to be provided for all the species and reactions of the model. Therefore, accurate and high-throughput methods to generate these data are required. In this work, we propose new methods to generate these data, and we apply them for the development of a detailed chemical kinetic model for n-butane autoxidation, which is then validated against literature data. Our approach for model development is based on the work of Jalan et al. [J. Phys. Chem. B 2013, 117, 2955-2970] who used Gibbs free energies of solvation [ΔsolvG(T)] to correct the data of the gas-phase kinetic model. In our approach, an equation of state (EoS) is used to compute ΔsolvG as a function of temperature for all the chemical species in the mechanism. Currently, ΔsolvG(T) of free radicals cannot be computed with an EoS and it was calculated for their parent molecule (H-atom added on the radical site). Theoretical calculations with the implicit solvent model were performed to quantify the impact of this assumption and showed that it is acceptable for radicals in n-butane and probably in all n-alkanes. New rate rules were proposed for the most important reactions of the model, based on theoretical calculations and the literature data. The developed detailed kinetic model for n-butane autoxidation is the first proposed model in the literature and was validated against the experimental data from the literature. Simulations showed that the main autoxidation products, sec-butyl hydroperoxides and 2-butanol, are produced from H-abstractions from n-butane by sec-C4H9OO radicals and the C4H9OO + C4H9OO reaction, respectively. The uncertainty of the product ratio ("butanone + 2-butanol"/"2-butoxy + 2-butoxy") of the latter reaction remains high in the literature, and our simulations suggest a 1:1 ratio in n-butane solvent.

Radical scavenger competition of alizarin and curcumin: a mechanistic DFT study on antioxidant activity

In vivo hydroxyl, peroxyl, and superoxide free radicals caused by oxidative stress can be toxic to molecules that are essential for the human body. However, there are natural compounds that can decrease the amount of these harmful species. In this work, we are focusing on two well-known compounds, alizarin (red) and curcumin, to study their interactions with these small radicals for a comparison between a rigid and a flexible structure. We made a mechanistic study and found the major and minor degradation products of curcumin as well as the autoxidation products of it based on a wide range of literature. We found several more favored pathways than those that were previously proposed. On the contrary, for degradation/oxidation of alizarin, only a few proposed mechanisms can be found which were performed in specific conditions. Our calculations predicted some favored rearrangements for the alizarin by peroxyl and superoxide radicals.Graphical abstractInteraction of alizarin red and bright yellow curcumin with small radicals like hydroxyl, peroxyl, and superoxide radicals, such as the reaction between curcumin radicals and oxygen molecule, results in different species like epoxides or another kind of radical forms. The stability of epoxides is different in the case of rigid and flexible structures.

The cholesterol autoxidation products, 7-ketocholesterol and 7β-hydroxycholesterol are associated with serum neurofilaments in multiple sclerosis

BackgroundSerum neurofilament light chain (sNfL) is an established marker of neuroaxonal injury in multiple sclerosis (MS). ObjectivesTo investigate if oxysterols produced from non-enzymatic and enzymatic cholesterol oxidation are differentially associated with sNfL measurements in MS. MethodsThis longitudinal study included 62 relapsing-remitting (RR-MS) and 36 progressive MS (PMS) patients with baseline and 5-year follow-up measures of serum levels of 6 oxysterols, sNfL and lipids. The oxysterols, 24-hydroxycholesterol (24HC), 25HC, 27HC, 7αHC, 7βHC and 7-ketocholesterol (7KC), were measured using liquid chromatography-mass spectrometry. sNfL was measured using single molecular array assay. Serum high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels were obtained from a lipid profile. ResultsThe enzymatically produced oxysterols 24HC, 25HC, 27HC and 7αHC were not associated with sNfL. However, baseline levels of reactive oxygen species (ROS) produced oxysterols, 7KC (p = 0.032) and 7βHC (p = 0.0025), were positively associated with sNfL levels at follow-up. Follow-up 7KC (p = 0.038) levels were also associated with follow-up sNfL levels. The associations of 7KC or 7βHC with sNfL remained significant after adjusting for LDL-C or HDL-C. Conclusions7KC and 7βHC, produced by ROS-mediated cholesterol oxidation are associated with neuroaxonal injury as assessed by sNfL in MS.

1205. Protectin D1 Induced by Clostridium butyricum MIYAIRI 588 Has an Anti-inflammatory Effects on Antibiotic-induced Intestinal Disorder

BackgroundThe administration of Clostridium butyricum MIYAIRI 588 (CBM 588) upregulates protectin D1,the anti-inflammatory lipid metabolites, in colon tissue under the antibiotic therapy. However, how CBM 588 induces protectin D1 nor whether the metabolite has anti-inflammatory effects on antibiotic-induced enteritis are unclear. Therefore, we evaluated the effect of CBM 588 on lipid metabolism and protectin D1 on immunological functions in colon tissue.MethodsMice were divided into five groups and clindamycin (CLDM), CBM 588 and/or protectin D1 were administered for 4 days (1. Control, 2. CLDM group, 3. CBM 588 group, 4. CLDM plus CBM 588 group and 5. CLDM plus protectin D1 group). After 4 days of administration, mice were reared for an additional 4 days. On day 8, colon tissues were removed to measure lipid metabolites with LC-MS/MS. Also, cytokines, lipid metabolism relative genes, enzymes were measured with qRT-PCR and ELISA.ResultsIn the CBM588 treatment group, protectin D1, α-linolenic acid, eicosapentaenoic acid (EPA) and autoxidation product of DHA (docosahexaenoic acid) were significantly increased, compared with CLDM group and control. At the same time, genes expression levels of polyunsaturated fatty acids (PUFAs) receptors, G-protein coupled receptor 120 (GPR120) and a DHA to protectin D1 metabolizing enzyme 15- lipoxygenase (LOX) in colon tissue increased. Il-4 produced by Th2 cells, also increased in CBM588 treated groups even under CLDM co-administration. In addition, similar to CBM 588, protectin D1 administration suppressed mice’s weight loss due to gut inflammation, decreased inflammatory cytokines, while anti-inflammatory cytokine IL-10 and TGF-β1 increased.PUFAs metabolism cascade induced by CBM 588. Lipid metabolism relative genes, pro/anti-inflammatory cytokines and body weight. ConclusionOur data suggested that CBM 588 stimulated PUFAs metabolism in the intestinal tract, and that PUFAs were signaled to Th2 cells as a ligand of GPR120. It was speculated that the stimulated Th2 cells produced IL4 and activated 15-LOX, resulting in the induction of protectin D1. Also, it became clear that protectin D1 induced anti-inflammatory cytokines in controlling antibiotic-induced gut inflammation. We provide as a new insight that lipid metabolism induction for the treatment of gut inflammatory diseases with CBM 588.Anti-inflammatory pathway of protectin D1 induced by CBM 588. Disclosures Hiroshige Mikamo, M.D, Ph.D, Astellas Pharma Inc. (Grant/Research Support, Speaker’s Bureau)MSD Japan (Grant/Research Support, Speaker’s Bureau)Pfizer Japan Inc. (Grant/Research Support)Sumitomo Dainippon Pharma Co., Ltd (Grant/Research Support, Speaker’s Bureau)

GC-MS approach revealing hidden nitrite reactions in hemolysate using 18O-labelled nitrite and cysteine-based thiols

In erythrocytes, nitric oxide (NO) and its autoxidation product nitrite undergo multiple reactions with hemoglobin species to form nitrate, Fe-nitrosyl hemoglobin (HbFe(II)NO), S-nitrosohemoglobin (HbCysβ93SNO), and other intermediates including nitrito-methemoblobin HbFe(III)ONO, nitro-methemoblobin HbFe(III)NO2 and nitrous anhydride (N2O3). Here, we report a stable-isotope dilution GC-MS assay that allows studying reactions of nitrite in hemolysate. The method is based on the use of 18O-labelled nitrite in combination with l-cysteine or N-acetyl-l-cysteine ethyl ester and GC-MS measurement of unlabelled and labelled nitrite and nitrate species. This approach reveals reactions that are hidden at physiological nitrite concentrations.

Antioxidant activity and synergism of canolol and α-tocopherol in rapeseed oil is affected by the presence of phospholipid association colloids

Interactions of canolol and α-tocopherol (α-T) with reverse micelles made from DOPC phospholipid (1,2-dioleoyl-sn-glycero-3-phosphocholine) in rapeseed oil were investigated in the current study. Furthermore, the antioxidant efficiency of canolol and α-T as well as the phenomenon of synergism between them in the oil containing association colloids has been determined. As demonstrated by fluorescence measurements, canolol may be incorporated into the structure of DOPC reverse micelles. This antioxidant may also accumulate in bulk oil at oil/water interface. In turn, no interactions of α-T with phospholipid association colloids were observed.The presence of DOPC association colloids affects antioxidant efficiency of canolol and α-T. Simultaneously, at the concentration 100 μmol of both substances, decreasing of their antioxidant activity effectiveness over time was observed. Formed during autoxidation amphiphilic compounds probably influence the structure of reverse micelles, modifying effectiveness of antioxidants. Antioxidant synergism of canolol and α-T occurs only in DOPC reverse micelles. Synergism phenomenon allows eliminating adverse effect of autoxidation products on the effectiveness of antioxidants. The presence of canolol may eliminate prooxidative action of α-T.

Electron ionization mass spectrometric fragmentation and detection of autoxidation products of 2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5-ene in Arctic sediments.

Some highly branched isoprenoid (HBI) alkenes are commonly used as proxies for palaeoceanographic reconstructions. However, there is a need to identify compounds that are sufficiently stable and abundant to be used as tracers of HBI oxidation in sediments. 2,6,10,14-Tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5(Z/E)-en-4-ols resulting from 2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5-ene appear to be useful for this purpose. Comparison of electron ionization (EI) mass spectra and retention times with those of standards allowed formal identification of autoxidation products of 2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5-ene. EI-MS fragmentations of TMS ethers of the main oxidation products (2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5(Z/E)-en-4-ols) were deduced by gas chromatography/electron ionization mass spectrometry (GC/EI-MS), low-energy collision-induced dissociation tandem mass spectrometry (CID-MS/MS) and accurate mass measurements. These compounds were then quantified in Arctic sediment samples in MS/MS multiple reaction monitoring (MRM) mode using transitions based on the main fragmentation pathways elucidated. 2,6,10,14-Tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5(Z/E)-en-4-ols were identified after autoxidation of the HBI alkene 2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5-ene. Low-energy CID-MS/MS analyses and accurate mass measurements allowed the EI-MS fragmentation pathways of their trimethylsilyl (TMS) derivatives to be elucidated. Some specific fragment ions and chromatographic retention times were also useful for further characterization. As an application of some of the described fragmentations, TMS derivatives of these metabolites were characterized and quantified in MRM mode in Arctic sediments. Due to their production in high proportions during autoxidation of their parent HBI diene, their apparent stability in sediments, and their specific EIMS fragmentations, (Z and E)-2,6,10,14-tetramethyl-7-(3-methylpent-4-enyl)-pentadec-5-en-4-ol TMS derivatives appeared to be useful tracers of HBI autoxidation in sediments.

On the Products of Cholesterol Autoxidation in Phospholipid Bilayers and the Formation of Secosterols Derived Therefrom.

In homogenous solution, cholesterol autoxidation leads to a mixture of epimers of 5 primary products, whose concentrations vary in the presence/absence of antioxidants, such as vitamin E. Two of the products (5α-OOH and 6β-OOH) undergo Hock fragmentation to yield electrophilic secosterols implicated in disease. Herein, we show that the product distribution is similar in phospholipid bilayers, in that the 7-OOHs are the major products, but the presence/absence of vitamin E has no effect on the distribution. Cholesterol 7α-OOH, but not 7β-OOH, undergoes Hock fragmentation to yield a mixture of unprecedented A-ring cleavage products and 6,7-epoxides. When subjected to typical derivatization conditions, 7α-OOH yields products with essentially indistinguishable chromatographic and spectroscopic features from the previously identified secosterols, casting further doubt on their controversial origin from endogenous O3 .

On the Products of Cholesterol Autoxidation in Phospholipid Bilayers and the Formation of Secosterols Derived Therefrom

AbstractIn homogenous solution, cholesterol autoxidation leads to a mixture of epimers of 5 primary products, whose concentrations vary in the presence/absence of antioxidants, such as vitamin E. Two of the products (5α‐OOH and 6β‐OOH) undergo Hock fragmentation to yield electrophilic secosterols implicated in disease. Herein, we show that the product distribution is similar in phospholipid bilayers, in that the 7‐OOHs are the major products, but the presence/absence of vitamin E has no effect on the distribution. Cholesterol 7α‐OOH, but not 7β‐OOH, undergoes Hock fragmentation to yield a mixture of unprecedented A‐ring cleavage products and 6,7‐epoxides. When subjected to typical derivatization conditions, 7α‐OOH yields products with essentially indistinguishable chromatographic and spectroscopic features from the previously identified secosterols, casting further doubt on their controversial origin from endogenous O3.

The Study of Mg(II) Ion Influence on Catechol Autoxidation in Weakly Alkaline Aqueous Solution

High performance liquid chromatography with diode array detection (HPLC-DAD) and electron spin resonance (ESR) spectroscopy were used to study Mg(II) ion influence on the autoxidation of catechol in weakly alkaline solution. The presence of Mg(II) ions greatly enhanced the catechol autoxidation rate and probably influenced the mechanism of reaction thus enabling formation of reaction products not obtained in the absence of metal ions. Consecutive formation of 1,2-benzoquinone, 2,3-oxanthrenediol, and 2,3-oxanthrenedione with intermediate o-semiquinone anion radicals during the initial stages of catechol autoxidation was suggested based on the detailed analysis of experimental HPLC-DAD and ESR data. The results of this study may help in better understanding of autoxidation of some biologically important catecholic molecules in real systems, where Mg(II) ions are ubiquitously present. Because of the possible toxicity of simple quinone molecules, it is important that the formation of relatively stable quinoid autoxidation products were detected in this study.

The Autoxidation of Alkenyl Succinimides—Mimics for Polyisobutenyl Succinimide Dispersants

Short chain alkenyl succinimides (ASIs) were synthesized and used as high purity chemical models to investigate the autoxidative degradation at 170 °C of polyisobutenyl succinimide dispersants (PIBSIs), a significant additive in automotive engine lubricants. Degradation products were characterized by gas chromatography–electron ionization mass spectrometry and quantified by gas chromatography-flame ionization detection. The rate of autoxidation of ASIs in a model lubricant, squalane, was also investigated. Although this is a complex molecule containing many possible sites of radical attack, all of the autoxidation products identified result from attack at the double bond or the adjacent allylic hydrogen atoms, which indicates the controlling influence of the double bond in the degradation of alkenyl succinimides, and therefore of commercial polyisobutenyl succinimide dispersants. The observed site-selective cleavage of the ASI structure, and by analogy PIBSI dispersants, would yield products that both reduce dispersancy and promote the formation of insoluble products that could have a detrimental effect on lubricant performance.