Oxidation Of Polyunsaturated Fatty Acids Research Articles

Role of Endogenous and Exogenous Tocopherols in the Lipid Stability of Marine Oil Systems: A Review.

In marine organisms primarily intended for human consumption, the quality of the muscle and the extracted oils may be affected by lipid oxidation during storage, even at low temperatures. This has led to a search for alternatives to maintain quality. In this sense, antioxidant compounds have been used to prevent such lipid deterioration. Among the most used compounds are tocopherols, which, due to their natural origin, have become an excellent alternative to prevent or retard lipid oxidation and maintain the quality of marine products. Tocopherols as antioxidants have been studied both exogenously and endogenously. Exogenous tocopherols are often used by incorporating them into plastic packaging films or adding them directly to fish oil. It has been observed that exogenous tocopherols incorporated in low concentrations maintain the quality of both muscle and the extracted oils during food storage. However, it has been reported that tocopherols applied at higher concentrations act as a prooxidant molecule, probably because their reactions with singlet oxygen may generate free radicals and cause the oxidation of polyunsaturated fatty acids in fish oils. However, when tocopherols are included in a fish diet (endogenous tocopherols), the antioxidant effect on the muscle lipids is more effective due to their incorporation into the membrane lipids, which can help extend the shelf life of seafood by reducing the lipid deterioration that occurs due to antioxidant synergy with other phenolic compounds used supplements in fish muscle. This review focuses on the most important studies in this field and highlights the potential of using tocopherols as antioxidants in marine oils.

Extra Virgin Olive Oil Reduced Polyunsaturated Fatty Acid and Cholesterol Oxidation in Rodent Liver: Is This Accounted for Hydroxytyrosol-Fatty Acid Conjugation?

The effects of extra virgin olive oil (EVOO) and carbon tetrachloride (CCl4) induced oxidative stress in rats were determined by the generation of isoprostanoids. These are known to be robust biomarkers to evaluate nonenzymatic and free radical related oxidation. Other oxidative stress biomarkers such as hydroxyeicosatetraenoic acid products (HETEs) and cholesterol oxidation products (COPs) were also determined. The rodents received a control diet, high-fat diet (20% w/w) composed of extra virgin olive oil (EVOO), corn oil (CO), or lard, and high-fat diets with CCl4 insult throughout the experimental period. The EVOO diet was found to suppress the formation of isoprostanoids and COPs compared to that of the control. EVOO also had a high total phenolic content and antioxidant activity compared to those of CO and lard and may be contributed to by the hydroxytyrosol component conjugated to fatty acids (HT-FA). This is the first study to identify HT-FA in EVOO, and it was 4-fold higher than that of olive oil, whereas none was found in corn oil. Furthermore, the EVOO diet showed reduced liver lipid vesicles in CCl4 treated rats compared to that of the control. However, liver toxicity measurements of AST (aspartate transaminase) and ALT (alanine transaminase) activities showed augmentation with CCl4 treatment but were not alleviated by the diets given. Our findings suggest that EVOO is a daily functional food capable of enhancing the antioxidant system for liver protection; the effect is potentially attributed to the phenolic and lipophenolic (phenol conjugated by fatty acids) content.

Full Library of (Bis–allyl)‐deuterated Arachidonic Acids: Synthesis and Analytical Verification

AbstractDeuteration at bis‐allylic positions slows down hydrogen abstraction, thereby reducing the rate of polyunsaturated fatty acids (PUFA) oxidation. Arachidonic acid undergoes oxidation through both enzymatic and non‐enzymatic mechanisms, giving rise to a range of important products with variable biological activity, including pro‐ and anti‐inflammatory properties. We report on the synthesis and verification of a full library of arachidonic acids variably deuterated at the bis‐allylic (C7, C10, C13) positions: 7,7‐D2‐arachidonic acid, 10,10‐D2‐arachidonic acid, 13,13‐D2‐arachidonic acid, 7,7,10,10‐D4‐arachidonic acid, 7,7,13,13‐D4‐arachidonic acid, 10,10,13,13‐D4‐arachidonic acid, and 7,7,10,10,13,13‐D6‐arachidonic acid isotopologues. The library is intended to be useful for determining the relative importance of enzymatic versus non‐enzymatic oxidation at particular sites in vivo.

Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis

Ferroptosis is form of regulated nonapoptotic cell death that is involved in diverse disease contexts. Small molecules that inhibit glutathione peroxidase 4 (GPX4), a phospholipid peroxidase, cause lethal accumulation of lipid peroxides and induce ferroptotic cell death. Although ferroptosis has been suggested to involve accumulation of reactive oxygen species (ROS) in lipid environments, the mediators and substrates of ROS generation and the pharmacological mechanism of GPX4 inhibition that generates ROS in lipid environments are unknown. We report here the mechanism of lipid peroxidation during ferroptosis, which involves phosphorylase kinase G2 (PHKG2) regulation of iron availability to lipoxygenase enzymes, which in turn drive ferroptosis through peroxidation of polyunsaturated fatty acids (PUFAs) at the bis-allylic position; indeed, pretreating cells with PUFAs containing the heavy hydrogen isotope deuterium at the site of peroxidation (D-PUFA) prevented PUFA oxidation and blocked ferroptosis. We further found that ferroptosis inducers inhibit GPX4 by covalently targeting the active site selenocysteine, leading to accumulation of PUFA hydroperoxides. In summary, we found that PUFA oxidation by lipoxygenases via a PHKG2-dependent iron pool is necessary for ferroptosis and that the covalent inhibition of the catalytic selenocysteine in Gpx4 prevents elimination of PUFA hydroperoxides; these findings suggest new strategies for controlling ferroptosis in diverse contexts.

Serum-Based Oxylipins Are Associated with Outcomes in Primary Prevention Implantable Cardioverter Defibrillator Patients.

IntroductionIndividuals with systolic heart failure are at risk of ventricular arrhythmias and all-cause mortality. Little is known regarding the mechanisms underlying these events. We sought to better understand if oxylipins, a diverse class of lipid metabolites derived from the oxidation of polyunsaturated fatty acids, were associated with these outcomes in recipients of primary prevention implantable cardioverter defibrillators (ICDs).MethodsAmong 479 individuals from the PROSE-ICD study, baseline serum were analyzed and quantitatively profiled for 35 known biologically relevant oxylipin metabolites. Associations with ICD shocks for ventricular arrhythmias and all-cause mortality were evaluated using Cox proportional hazards models.ResultsSix oxylipins, 17,18-DiHETE (HR = 0.83, 95% CI 0.70 to 0.99 per SD change in oxylipin level), 19,20-DiHDPA (HR = 0.79, 95% CI 0.63 to 0.98), 5,6-DiHETrE (HR = 0.73, 95% CI 0.58 to 0.91), 8,9-DiHETrE (HR = 0.76, 95% CI 0.62 to 0.95), 9,10-DiHOME (HR = 0.81, 95% CI 0.65 to 1.00), and PGF1α (HR = 1.33, 95% CI 1.04 to 1.71) were associated with the risk of appropriate ICD shock after multivariate adjustment for clinical factors. Additionally, 4 oxylipin-to-precursor ratios, 15S-HEPE / FA (20:5-ω3), 17,18-DiHETE / FA (20:5-ω3), 19,20-DiHDPA / FA (20:5-ω3), and 5S-HEPE / FA (20:5-ω3) were positively associated with the risk of all-cause mortality.ConclusionIn a prospective cohort of patients with primary prevention ICDs, we identified several novel oxylipin markers that were associated with appropriate shock and mortality using metabolic profiling techniques. These findings may provide new insight into the potential biologic pathways leading to adverse events in this patient population.

Mass spectrometry-based proteomics of oxidative stress: Identification of 4-hydroxy-2-nonenal (HNE) adducts of amino acids using lysozyme and bovine serum albumin as model proteins.

Modification of proteins by 4-hydroxy-2-nonenal (HNE), a reactive by-product of ω6 polyunsaturated fatty acid oxidation, on specific amino acid residues is considered a biomarker for oxidative stress, as occurs in many metabolic, hereditary, and age-related diseases. HNE modification of amino acids can occur either via Michael addition or by formation of Schiff-base adducts. These modifications typically occur on cysteine (Cys), histidine (His), and/or lysine (Lys) residues, resulting in an increase of 156 Da (Michael addition) or 138 Da (Schiff-base adducts), respectively, in the mass of the residue. Here, we employed biochemical and mass spectrometry (MS) approaches to determine the MS "signatures" of HNE-modified amino acids, using lysozyme and BSA as model proteins. Using direct infusion of unmodified and HNE-modified lysozyme into an electrospray quadrupole time-of-flight mass spectrometer, we were able to detect up to seven HNE modifications per molecule of lysozyme. Using nanoLC-MS/MS, we found that, in addition to N-terminal amino acids, Cys, His, and Lys residues, HNE modification of arginine (Arg), threonine (Thr), tryptophan (Trp), and histidine (His) residues can also occur. These sensitive and specific methods can be applied to the study of oxidative stress to evaluate HNE modification of proteins in complex mixtures from cells and tissues under diseased versus normal conditions.

Membranes as Structural Antioxidants: RECYCLING OF MALONDIALDEHYDE TO ITS SOURCE IN OXIDATION-SENSITIVE CHLOROPLAST FATTY ACIDS

Genetic evidence suggests that membranes rich in polyunsaturated fatty acids (PUFAs) act as supramolecular antioxidants that capture reactive oxygen species, thereby limiting damage to proteins. This process generates lipid fragmentation products including malondialdehyde (MDA), an archetypal marker of PUFA oxidation. We observed transient increases in levels of endogenous MDA in wounded Arabidopsis thaliana leaves, raising the possibility that MDA is metabolized. We developed a rigorous ion exchange method to purify enzymatically generated (13)C- and (14)C-MDA. Delivered as a volatile to intact plants, MDA was efficiently incorporated into lipids. Mass spectral and genetic analyses identified the major chloroplast galactolipid: α-linolenic acid (18:3)-7Z,10Z,13Z-hexadecatrienoic acid (16:3)-monogalactosyldiacylglycerol (18:3-16:3-MGDG) as an end-product of MDA incorporation. Consistent with this, the fad3-2 fad7-2 fad8 mutant that lacks tri-unsaturated fatty acids incorporated (14)C-MDA into 18:2-16:2-MGDG. Saponification of (14)C-labeled 18:3-16:3-MGDG revealed 84% of (14)C-label in the acyl groups with the remaining 16% in the head group. 18:3-16:3-MGDG is enriched proximal to photosystem II and is likely a major in vivo source of MDA in photosynthetic tissues. We propose that nonenzymatically generated lipid fragments such as MDA are recycled back into plastidic galactolipids that, in their role as cell protectants, can again be fragmented into MDA.

Abstract 227: The Role of Fatty Acid Desaturase 1 in Inflammation Initiation and Resolution in Atherosclerosis

Studies suggest that dietary enrichment of polyunsaturated fatty acids (PUFAs) may improve CVD outcomes, however the mechanisms underlying these observations remain elusive. Additionally, genome-wide association studies have linked single nucleotide polymorphisms (SNPs) in genes encoding essential PUFA metabolizing enzymes, the Fatty Acid Desaturases 1, 2, and 3 ( FADS1-2-3 ), to dyslipidemia and other metabolic risk factors known to be linked to CVD. Since enzymatic oxidation of specific PUFAs, commonly arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), generate signaling mediators that coordinate both the initiation and resolution of inflammation, understanding the interplay of PUFA metabolism and vascular inflammation has broad implications in cardiometabolic drug discovery. Here we have altered the abundances of distinct dietary and endogenously-synthesized PUFAs, and associated lipid mediators, in hyperlipidemic Ldlr-/- mice to understand the signaling mechanisms underlying the PUFA-CVD link. We diversified PUFA profiles by feeding diets enriched in either ω-6 or ω-3 PUFAs, and inhibited endogenous production of AA and EPA by antisense oligonucleotide (ASO)-mediated knockdown of the Δ5 desaturase Fads1. Fads1 knockdown results in accumulation of its substrate fatty acids (dihomo-γ-linolenic acid and eicosatrienoic acid) and marked reduction in its enzymatic products (AA and EPA). Metabololipidomic profiling reveals that Fads1 knockdown alters select AA-, EPA-, and DHA-derived lipid mediators in a diet-specific manner. Interestingly, Fads1 knockdown protects Ldlr-/- mice from obesity and insulin resistance regardless of diet, yet alters increases circulating monocyte subsets and promotes dyslipidemia in a highly diet-specific manner. How these phenotypes link to diet-induced atherosclerosis burden in Fads1 knockdown mice will also be presented. Collectively, our studies provide new information in regards to the relative contribution of endogenous (FADS1-derived) and exogenous (diet-derived) AA and EPA in driving cardiometabolic phenotypes. Furthermore, our studies provide the first mechanistic understanding behind the genetic link of FADS1-2-3 SNPs and atherosclerosis.

Protective effects of azarole polyphenolic extracts against oxidative damage using in vitro biomolecular and cellular models

The antioxidant activity of the different polyphenolic extracts prepared from Tunisian azarole, Crataegus azarolus and Crataegus monogyna (Rosaceae family) leaves, fruit peel, pulp and syrup was evaluated using cholesterol, liposome and rat liver-homogenate oxidation assays and cytotoxic activity in differentiated Caco-2, undifferentiated Caco-2, and B16F10 melanoma cells. Protective effects were observed against thermal-cholesterol degradation at 140°C for 1h, which depended on the concentration and the type of the extract. Moreover, the pre-treatment with the phenolic extracts preserved liposomes and rat liver-homogenate from oxidative induced damage by Cu2+ and Fe2+ at 37°C for 24h and 2h, respectively. Azarole phenolics inhibited the oxidation of polyunsaturated fatty acids (PUFA) and limited the production of oxidized compounds. Furthermore, within tested concentrations (0.24-4.8mg/mL), all extracts did not show any toxic effect on differentiated Caco-2 cells; while, they were found cytotoxic to cancer Caco-2 cells, except, extracts of pulp and syrup of C. monogyna. Using B16F10 melanoma cell model, only azarole pulp and syrup extracts were found toxic and induced the production of melanin in a dose-dependent manner.

Comparative Effects of Glutathione Peroxidase‐1 Overexpression and Cu/Zn‐superoxide Dismutase Knockout on Murine Hepatic Fatty Acid Metabolism

Glutathione peroxidase‐1 (GPX1) and Cu/Zn‐superoxide dismutase (SOD1) are two major antioxidant enzymes, while polyunsaturated fatty acids (PUFA) including eicosapentaenoic acid (20:5n‐3, EPA) and docosahexaenoic acid (22:6n‐3, DHA) are health‐promoting nutrients. This study was conducted to determine the effects of GPX1 overexpression and SOD1 knockout on hepatic synthesis, accumulation, and oxidation of PUFA. GPX1 overexpressing (OE, 6–7 mo), and SOD1 knockout (SKO, 2 mo) mice and their respective wild‐type controls were fed a Torula yeast basal diet supplemented with 0 or 5% defatted microalgae (Nannochloropsis oceanica, 16% EPA) for 8 wk (n = 5 to 7 per group). Overexpression of GPX1 decreased (P < 0.01) linoleic acid (18:2n‐6) concentration and raised (P < 0.05) ω‐3/ω‐6 fatty acid ratio in the liver of mice regardless of diets. In comparison, knockout of SOD1 decreased (P < 0.05) concentrations of PUFA, in particular eicosatrienoic acid (20:3n‐3, precursor of EPA) and DHA, in mice fed both diets. The knockout of SOD1 also resulted in lower (P < 0.01) hepatic ω‐3/ω‐6 fatty acid ratio than the wild‐type mice when both genotypes were fed the algae diet. Inclusion of 5% algae in the diet elevated (P < 0.05) the hepatic DHA concentration in only wild‐type mice of SOD1. Results of qPCR analysis showed that knockout of SOD1 down‐regulated (P < 0.05) hepatic mRNA levels of elongase 2 and 5, the major enzymes involved in long chain PUFA synthesis, compared with the wild‐type controls. Meanwhile, the OE mice had lower (P < 0.05) hepatic mRNA levels of PUFA oxidation‐related genes including cyclooxygenase 1 (COX1), COX2, and arachidonate 5‐lipoxygenase than their wild‐type controls. In addition, feeding the algae diet decreased (P < 0.01) non‐esterified fatty acid concentrations in both plasma and liver of the OE mice, and concentration of triglycerides in the liver of the SOD1 wild‐type mice. In conclusion, overexpression of GPX1 and knockout of SOD1 exerted differential effects on synthesis, accumulation and oxidation of hepatic PUFA in mice. Further study requires to measure oxidized metabolites of PUFA and to reveal molecular mechanisms by which GPX1 and SOD1 regulate PUFA metabolism.Support or Funding InformationSupported in part by a NIH grant DK53018 and a USDA/DOE Biomass R&D Initiative Grant

The role of 12/15‐Lipoxygenase in a Mouse Model of Alcoholic Liver Disease

Introduction/Aim12/15‐Lipoxygenase (12/15‐LOX) catalyzes the oxidation of free and esterified polyunsaturated fatty acids, predominantly, linoleic and arachidonic, generating the whole spectrum of bioactive lipid mediators. This enzyme is involved in the regulation of various homeostatic processes as well as in the pathogenesis of multiple diseases. Recently published studies from our group and others have shown that experimental and clinical alcoholic liver disease was associated with elevated oxidized linoleic acid metabolites (OXLAMs), specifically 9‐ and 13‐hydroxy‐octadecadienoic acids (9‐ and 13‐HODEs). The aim of the present study was to examine the role of 12/15‐LOX in an animal model of ALD.Materials and MethodsEight‐week‐old male 12/15‐LOX knockout mice (12/15‐LOX−/−), and their genetically unaltered wild type (WT) counterparts were fed Lieber–DeCarli control (isocaloric maltose‐dextrin) or ethanol (5% w/v) liquid diets ad libitum for 10 days plus a single binge ethanol administration (5 g/kg) by gavage, whereas mice in control groups were gavaged with isocaloric maltose dextrin. Liver histopathological changes were estimated by hematoxylin and eosin staining. Liver triglyceride accumulation was assessed by biochemical assay and Oil Red O staining. Liver injury was evaluated by plasma ALT and AST activity. Liver inflammation was determined by hepatic proinflammatory gene expression. Chloroacetate esterase staining was used to evaluate necroinflammatory changes. TUNEL staining was used to determine hepatic apoptotic cell death. Plasma OXLAMs were analyzed on LC‐MS and GCxGC/TOF‐MS platforms.ResultsChronic‐binge alcohol administration resulted in a marked increase in plasma OXLAM levels, specifically 9‐HODE and 13‐HODE, in parallel with up‐regulation of hepatic 12/15‐LOX in WT animals. These effects were associated with hepatic steatosis, inflammation and injury. 12/15‐LOX genetic depletion did not reduced hepatic steatosis caused by EtOH, but did ameliorate hepatic injury as assessed by ALT (231.2+32.8 U/L in WT vs 148.4+48.6 U/L in 12/15‐LOX−/−) and AST (279.1+36.7 U/L in WT vs 177.1+28.3 U/L in 12/15‐LO−/−) levels. 12/15‐LOX deficiency did not affect hepatic apoptosis; while neutrophil infiltration was significantly reduced in 12/15‐LOX deficient mice compared to WT animals. 12/15‐LOX deficiency prevented EtOH‐induced pro‐inflammatory cytokine and chemokine expression, including Tnf‐α and Mcp1 mRNA levels.Conclusion12/15 LOX plays an important role in the pathogenesis of experimental ALD, in part, via increased production of OXLAMs. 12/15‐LOX and OXLAMs may represent novel therapeutic targets in ALD managementSupport or Funding InformationStudy supported by the NIH and Veterans Administration.

Targeting Reactive Carbonyl Species with Natural Sequestering Agents.

Reactive carbonyl species generated by the oxidation of polyunsaturated fatty acids and sugars are highly reactive due to their electrophilic nature, and are able to easily react with the nucleophilic sites of proteins as well as DNA causing cellular dysfunction. Levels of reactive carbonyl species and their reaction products have been reported to be elevated in various chronic diseases, including metabolic disorders and neurodegenerative diseases. In an effort to identify sequestering agents for reactive carbonyl species, various analytical techniques such as spectrophotometry, high performance liquid chromatography, western blot, and mass spectrometry have been utilized. In particular, recent advances using a novel high resolution mass spectrometry approach allows screening of complex mixtures such as natural products for their sequestering ability of reactive carbonyl species. To overcome the limited bioavailability and bioefficacy of natural products, new techniques using nanoparticles and nanocarriers may offer a new attractive strategy for increased in vivo utilization and targeted delivery of bioactives.

Lipid modification processes induced by thiyl radicals

Polyunsaturated fatty acid (PUFA) oxidation by thiyl radicals (RS•) is believed to be responsible for some of the biological radiation damage. At the same time, RS• can cause isomerization of PUFA double bonds with the formation of trans isomers. The aim of this study was to better understand the competition between lipid peroxidation and geometrical isomerization processes in biomimetic model system of linoleic acid in the presence of 2-mercaptoethanol using irradiation as a method for free radicals generation. In air-equilibrated conditions the propagation of lipid peroxidation was dominant up to the dose of 400Gy, after which at higher doses up to 10kGy the termination occurred with the predominance of geometrical isomerization. This study revealed that undesirable and permanent lipid modifications are possible at higher irradiation doses which should be considered in the planning of irradiation treatment of foods and feeds with high content of lipids and sulfur compounds.

A Revised Mechanism for Human Cyclooxygenase-2

The mechanism of ω-6 polyunsaturated fatty acid oxidation by wild-type cyclooxygenase 2 and the Y334F variant, lacking a conserved hydrogen bond to the catalytic tyrosyl radical/tyrosine, was examined for the first time under physiologically relevant conditions. The enzymes show apparent bimolecular rate constants and deuterium kinetic isotope effects that increase in proportion to co-substrate concentrations before converging to limiting values. The trends exclude multiple dioxygenase mechanisms as well as the proposal that initial hydrogen atom abstraction from the fatty acid is the first irreversible step in catalysis. Temperature dependent kinetic studies reinforce the novel finding that hydrogen transfer from the reduced catalytic tyrosine to a terminal peroxyl radical is the first irreversible step that controls regio- and stereospecific product formation.

Oxidation of Polyunsaturated Fatty Acids and its Impact on Food Quality and Human Health

Oxidation of Polyunsaturated Fatty Acids and its Impact on Food Quality and Human Health

Heme iron in meat as the main source of iron in the human diet

Iron is a trace element involved in many cardinal metabolic processes of almost all living organisms. It is well known that iron participates in oxygen transport as well as it is a cofactor in many fundamental enzymatic and nonenzymatic processes. Accordingly, disturbances of iron homeostasis can cause serious clinical consequences. In humans, dietary iron can enter the body in two main forms: heme and nonheme. The former is a component of many hemoproteins (including myoglobin, hemoglobin, cytochromes b and c) and is easily absorbed in the duodenal enterocytes. Red meat is an excellent source of heme iron, while the less bioavailable nonheme form is found in large amounts in milk products and vegetables. For this reason, consumers of meat have a better iron status than vegetarians and vegans. Heme iron found in muscle protein should be supplied to humans to prevent iron deficiency, which can lead to anemia. It is easily absorbed and its main source is red meat. In addition, heme iron, which is mainly found in myoglobin in meat, contributes to the desirable bright red color and to the most undesirable brown color of meat. Both heme and nonheme iron are catalysts of lipid oxidation in meat. This process lowers the nutritive value through oxidation of polyunsaturated fatty acids, which produces an undesirable flavor and aroma. The aim of this paper was to discuss the role of heme iron in the human diet.

Amounts of the reactive aldehydes, malonaldehyde, 4‐hydroxy‐2‐hexenal, and 4‐hydroxy‐2‐nonenal in fresh and oxidized edible oils do not necessary reflect their peroxide and anisidine values

There is a growing development of foods and food supplements enriched in n‐3 lipids, whereas quantitative data on oxidation products present throughout the food chain are lacking. To give a first insight of the range of potentially toxic aldehydes that can be encountered in these foods, malondialdehyde (MDA), 4‐hydroxy‐2‐hexenal (4‐HHE) and 4‐hydroxy‐2‐nonenal (4‐HNE) were quantified in a set of four fresh and oxidized oils presenting large variations in unsaturation levels, n‐6/n‐3 ratio and oxidabilities. Results were compared to classical methods. In fresh rapeseed, sunflower, kiwiseed, and tuna oils, the concentrations of MDA ranged between 0.6 and 29 μmol kg−1 oil, of hydroxyalkenals between 0.1 and 3.3 μmol kg−1, hydroperoxides concentrations (HPX) ranged between 0.4 and 4 mmol kg−1 oil, peroxide value (PV) and anisidine value (AV) were well below the acceptable limits. In oxidized rapeseed, kiwiseed, and tuna oils 4‐HHE ranged from 120 to 150 μmol kg−1, whereas MDA ranged from 600 to above 1100 μmol kg−1. Conversely, sunflower oil exhibited the highest quantities 4‐HNE (175 μmol kg−1) but the lowest of MDA (100 μmol kg−1) and 4‐HHE (2.9 μmol kg−1) in agreement with its fatty chain composition. Altogether, the results highlight the interest of using methods able to quantify specific oxidation products and not only PV and AV to assess lipid oxidation especially in oils or products containing high quantities of n‐3 FA.Practical applications: This work provides quantitative data regarding amounts of toxic aldehydes that can be present in edible oils. The used methods made it possible to quantify MDA, 4‐HNE, and 4‐HHE as respective markers of oxidation of polyunsaturated fatty acids in a whole, n‐6 and n‐3 polyunsaturated fatty acids. They could be applied to oils, fats, and food products to better estimate the occurrence and exposure to these compounds. Comparison with methods currently used to evaluate the quality of edible oils indicates clearly that the dynamics of formation of the different oxidation markers are oil‐specific. Thus, oxidation indicators should be selected as regard to fatty chain profiles and not used to compare oils with very different profiles of polyunsaturated fatty acids .These tools could be used to design nutritional, metabolic, and toxicological trials avoiding too unrealistic exposures in undesirable contaminants.MDA, 4‐HNE, and 4‐HHE were quantified in fresh and oxidized rapeseed, sunflower (S), kiwiseed (K) and tuna oils (T), together with classical (R) markers such as PV or CD. In fresh oils, MDA ranged from 0.6 up to 29 µmol kg−1 oil, whereas 4‐HNE and 4‐HHE were closed to 1 µmol kg−1 oil whatever the oil, excepted in fresh kiwiseed oil (3.3 µmol kg−1 oil). MDA was the major secondary product in highly oxidized oils except in sunflower oil. Its quantities ranged from 100 µmol kg−1 in sunflower up to 1.1 mmol kg−1 in kiwiseed oil. 4‐HNE is the major secondary product in sunflower oil (170 µmol kg−1), while 4‐HHE ranged from 120 to 150 µmol kg−1 in n‐3 containing oils. The evolution of marker profiles is oil‐specific.

Novel non-methylated furan fatty acids in fish from a zero discharge aquaculture system

BackgroundFuran fatty acids (F-acids) are valuable minor fatty acids which are appraised for their protective role against lipid oxidation of polyunsaturated fatty acids (PUFAs). The most relevant dietary source for F-acids is fish with the predominant occurrence of up to five dimethyl- or monomethyl-substituted homologues. During the screening of fish from a zero discharge aquaculture (ZDA) system we noted the potential presence of unusual F-acids. MethodsWe developed a method by gas chromatography with mass spectrometry operated in the selected ion monitoring mode for elucidation of the structures of the uncommon F-acids. ResultsCarp from the ZDA system contained seven non-methylated F-acids with dominance of 8-(5-hexylfuran-2-yl)-octanoic acid (8F6). Non-methylated F-acids have never been detected before in fish. Subsequent analysis of other fish species and a batch of the fish feed confirmed the presence of non-methylated F-acids. ConclusionsF-acids in fish are derived from the feed. Our investigation indicates that more emphasis should be put on the F-acid concentrations in fish from aquaculture, which appears to depend on the quality of the fish feed.

Antioxidant Role for Lipid Droplets in a Stem Cell Niche of Drosophila

SummaryStem cells reside in specialized microenvironments known as niches. During Drosophila development, glial cells provide a niche that sustains the proliferation of neural stem cells (neuroblasts) during starvation. We now find that the glial cell niche also preserves neuroblast proliferation under conditions of hypoxia and oxidative stress. Lipid droplets that form in niche glia during oxidative stress limit the levels of reactive oxygen species (ROS) and inhibit the oxidation of polyunsaturated fatty acids (PUFAs). These droplets protect glia and also neuroblasts from peroxidation chain reactions that can damage many types of macromolecules. The underlying antioxidant mechanism involves diverting PUFAs, including diet-derived linoleic acid, away from membranes to the core of lipid droplets, where they are less vulnerable to peroxidation. This study reveals an antioxidant role for lipid droplets that could be relevant in many different biological contexts.

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Furan (C4H4O) is a volatile compound formed mostly during the thermal processing of foods. The toxicity of furan has been well documented previously, and it was classified as “possible human carcinogen (Group 2B)” by the International Agency for Research on Cancer. Various pathways have been reported for the formation of furan, that is, thermal degradation and/or thermal rearrangement of carbohydrates in the presence of amino acids, thermal degradation of certain amino acids, including aspartic acid, threonine, α-alanine, serine, and cysteine, oxidation of ascorbic acid at higher temperatures, and oxidation of polyunsaturated fatty acids and carotenoids. Owing to the complexity of the formation mechanism, a vast number of studies have been published on monitoring furan in commercial food products and on the potential strategies for reducing furan. Thus, we present a comprehensive review on the current status of commercial food monitoring databases and the possible furan reduction methods. Additionally, we review analytical methods for furan detection and the toxicity of furan.