Phospholipid Oxidation Research Articles

Exploring the contribution of phosphatidylcholine and triglyceride on the formation of beef aroma-active compounds with thermal oxidation system.

Thermal oxidation of phospholipids and triglycerides is a major source of beef aroma compounds. In this study, phosphatidylcholine (PC) and triglyceride (TG) were isolated and purified from beef and added to defatted beef and raw beef. The composition of aroma compounds generated by thermal oxidation in three model systems were compared by flavoromics. The main aroma compounds produced by the thermal oxidation of PC were decanal, (E)-2-nonenal, (E)-2-undecenal, and (E,E)-2,4-decadienal, while the main aroma compounds produced by the thermal oxidation of TG were nonanal, (E)-2-undecenal, and decanal. Nonanal remains the main aroma compound produced by PC and TG in defatted beef. Octanal and nonanal were the major aroma compounds generated by thermal oxidation of raw beef samples spiked with PC and TG. Raw beef with added PC and TG had higher levels of sulfides and heterocycles after thermal oxidation compared to defatted beef with added lipids. The comparison of the aroma profiles in three thermo-oxidative models indicated that PC contributed more than TG to the key odor-active compounds in cooked beef. Additionally, the thermo-oxidative degradation of PC facilitated the formation of Maillard reaction products. However, the beef matrix may inhibit the formation of decanal and (E,E)-2,4-decadienal.

Possible Missing Sources of Atmospheric Glyoxal Part I: Phospholipid Oxidation from Marine Algae.

Glyoxal has been implicated as a significant contributor to the formation of secondary organic aerosols, which play a key role in our ability to estimate the impact of aerosols on climate. Elevated concentrations of glyoxal over remote ocean waters suggests that there is an additional source, distinct from urban and forest environments, which has yet to be identified. Herein, we demonstrate that the ocean can serve as an appreciable source of glyoxal in the atmosphere due to microbiological activity. Based on mass spectrometric analyses of nascent sea spray aerosols and the sea surface microlayer (SSML) of naturally occurring algal blooms, we provide evidence that during the algae death phase phospholipids become enriched in the SSML and undergo autoxidation thereby generating glyoxal as a degradation product. We propose that the death phase of an algal bloom could serve as an important and currently missing source of glyoxal in the atmosphere.

Electroformation and characterization of soybean protein isolate hydrolysates-modified liposomes

This research aimed to elucidate the application and feasibility of the enhancement of liposome oxidative stability by the interaction of liposomes with soybean protein isolate hydrolysates (SPIHs) during liposome electroformation. It was observed that the degree of hydrolysis, percentage of low-molecular-weight distribution, and solubility of SPIHs after enzymatic hydrolysis increased with the extension of reaction time. The average fluorescence intensity (average gray level) was approximately 200 a.u. for each liposome, indicating a homogeneous distribution of SPIHs on the liposome surface. Moreover, it was found that the advanced structure of SPIHs incorporated with liposomes was altered appreciably. Both hydrophobic forces and hydrogen bonds exhibited an important role in the interaction between SPIHs and liposomes. In addition, morphology observation indicated that the liposomes were spherical and exhibited a more compact structure after coating with SPIHs. Subsequent flow cytometry analysis showed that the diameter and number of vesicles would increase due to vesicles rupturing or reorganizing after phospholipid oxidation during the electroformation of liposomes to produce SPIHs-liposomes. While the phospholipid oxidation level of the original liposomes was 42.13%, the phospholipid oxidation level of SPIHs-liposomes did not exceed 25%, indicating that the optimal balance between electroformation parameters and phospholipid oxidation level was obtained. These results may provide novel insight into the implications of SPIHs-modified liposomes as functional additives.

Ferroptosis: Potential therapeutic targets and prognostic predictions for acute myeloid leukemia (Review).

Ferroptosis is a relatively recently discovered type of regulated cell death that is induced by iron-dependent lipid peroxidation. The key contributing factors to ferroptosis are the loss of glutathione peroxidase 4 which is required for reversing lipid peroxidation, the buildup of redox-active iron and the oxidation of phospholipids containing polyunsaturated fatty acids. Ferroptosis has been associated with a number of diseases, including cancers such as hepatocellular carcinoma, breast cancer, acute renal damage and neurological disorders such as Alzheimer's disease and Alzheimer's disease, and there may be an association between ferroptosis and acute myeloid leukemia (AML). The present review aims to describe the primary regulatory pathways of ferroptosis, and the relationship between ferroptosis and the occurrence and development of AML. Furthermore, the present review comprehensively summarizes the latest advances in the treatment and prognosis of ferroptosis in AML.

Nickel-induced oxidative stress and phospholipid remodeling in cucumber leaves

Nickel phytotoxicity has been attributed, among others, to oxidative stress. However, little is known about Ni-induced phospholipid modifications, including the oxidative ones. Accumulation of reactive oxygen species (ROS), antioxidative enzyme activities, malondialdehyde and the early lipid oxidation products contents, membrane permeability, phospholipid profile as well as phospholipid unsaturation degree were studied in the 1st and the 2nd leaves of hydroponically grown cucumber seedlings subjected to Ni stress. Compared to the 2nd leaf the 1st one showed stronger visual Ni toxicity symptoms, higher Ni, O2.- and H2O2 accumulation as well as greater enhancement in membrane permeability. Enzyme activities were differently influenced by Ni stress, however most pronounced changes were generally found in the 1st leaf. Ni treatment resulted in oxidation of leaf lipids, which was evidenced by appearance of increased contents of MDA and the early produced oxylipins. Among the latter 9-hydroxyoctadecatrienoic acid (9-HOTrE) and 13-hydroxyoctadecatrienoic acid (13-HOTrE) contents showed the most pronounced increase in response to Ni treatment. Exposure to the metal led to the changes in the leaf phospholipid profile and increased degree of phospholipid unsaturation. The obtained results have been discussed in relation to the difference in Ni stress severity between the 1st and the 2nd leaves.

The influence mechanism of phospholipids structure and composition changes caused by oxidation on the formation of flavor substances in sturgeon caviar

The oxidation-induced phospholipids (PLs) underwent structural and compositional analysis, alongside the establishment of a simulation system to verify the link between phospholipid oxidation and flavor substances formation in sturgeon caviar. Structural alterations of PLs were tracked using 31P and 1H nuclear magnetic resonance (NMR), electron spin resonance spectroscopy (ESR), and Raman spectroscopy. The findings revealed a reduction in phosphatidylcholine (PC) and phosphatidylethanolamine (PE) from 82.3% and 10.4% to 58.2% and 5.8% respectively. Free radical signals exhibited an initial increase followed by a decrease. The diminished intensity in Raman spectra at 970 and 1080 cm−1 indicated reduced fat unsaturation attributable to PLs oxidation. Correlation analysis highlighted a significant association between PC and PE containing C22:6, C20:5, C20:4, and C18:2 with flavor substances, suggesting their role as key precursors for flavor development. This study established a theoretical basis for understanding the change of flavor quality in sturgeon caviar during storage.

Oxidized Phospholipids Regulate Tenocyte Function via Induction of Amphiregulin in Dendritic Cells.

Inflammation is a driving force of tendinopathy. The oxidation of phospholipids by free radicals is a consequence of inflammatory reactions and is an important indicator of tissue damage. Here, we have studied the impact of oxidized phospholipids (OxPAPC) on the function of human tenocytes. We observed that treatment with OxPAPC did not alter the morphology, growth and capacity to produce collagen in healthy or diseased tenocytes. However, since OxPAPC is a known modulator of the function of immune cells, we analyzed whether OxPAPC-treated immune cells might influence the fate of tenocytes. Co-culture of tenocytes with immature, monocyte-derived dendritic cells treated with OxPAPC (Ox-DCs) was found to enhance the proliferation of tenocytes, particularly those from diseased tendons. Using transcriptional profiling of Ox-DCs, we identified amphiregulin (AREG), a ligand for EGFR, as a possible mediator of this proliferation enhancing effect, which we could confirm using recombinant AREG. Of note, diseased tenocytes were found to express higher levels of EGFR compared to tenocytes isolated from healthy donors and show a stronger proliferative response upon co-culture with Ox-DCs, as well as AREG treatment. In summary, we identify an AREG-EGFR axis as a mediator of a DC-tenocyte crosstalk, leading to increased tenocyte proliferation and possibly tendon regeneration.

Oxidized phospholipids regulate tenocyte function via the induction of amphiregulin in dendritic cells

Abstract Inflammation is a driving force of tendinopathy. Oxidation of phospholipids by free radicals is a consequence of inflammatory reactions. Here we have studied the impact of oxidized phospholipids (OXPAPC) on the function of human tenocytes. We observed that treatment with OXPAPC did not alter the morphology, growth, and capacity to produce collagen in healthy or diseased tenocytes. Since OXPAPC is a known modulator of the function of immune cells, we analyzed whether OXPAPC-treated immune cells might influence the fate of tenocytes. Treatment of immature, monocyte-derived dendritic cells with OXPAPC (Ox-DCs) was found to enhance the proliferation of tenocytes, in particular tenocytes from diseased tendons. In contrast, the production of collagen by tenocytes was not altered upon co-culture with Ox-DCs. Since the supernatant of Ox-DCs was also able to stimulate the growth of tenocytes, we searched for a growth factor in the secretome of Ox-DCs and could identify amphiregulin (AREG), a ligand for EGFR. The addition of recombinant AREG to tenocytes was indeed a stimulus of proliferation. Diseased tenocytes were found to express higher levels of EGFR compared to tenocytes isolated from healthy donors and show a stronger proliferative response. In summary, inflammatory reactions in the tendon might lead to the oxidation of phospholipids which can trigger the production of AREG in resident DCs and thereby stimulate the proliferation of tenocytes.

Abstract 3093: Can Inhibiting Ferroptosis And Subsequent Endothelial Glycocalyx Shedding Reduce The Morbidity And Mortality Of Hemorrhagic Shock?

Background: Trauma patients with hemorrhagic shock accounts for 40% of preventable death. Shock-induced endotheliopathy has garnered interest recently and one aspect of this, endothelial glycocalyx shedding, has shown to promote coagulopathy following hemorrhage. Ferroptosis is an iron dependent, non-apoptotic form of controlled cell death triggered by the oxidation of membrane phospholipids. Liproxstatin-1 (LPX1) is an inhibitor of this process and can protect against oxidative damage to the endothelial cell membrane and subsequent shedding of glycocalyx. We hypothesized that LPX1 would reduce endothelial glycocalyx damage in hemorrhagic shock. Methods: A rat model of hemorrhagic shock and resuscitation was used to assess glycocalyx disruption in the lungs via fluorescent-labeled wheat germ agglutinin staining in frozen tissue and by Syndecan-1 ELISA on plasma samples. A control group (n=5) resuscitated only with Lactated Ringer’s solution, following hemorrhage and resuscitation (H/R) was compared against an experimental group (n=5) that received LPX1 following hemorrhage and before resuscitation. Results: Glycocalyx shedding (assessed by an increase in plasma Syndecan-1 levels) was prevented in the LPX1 treated group compared to control group. Lung tissue staining of the glycocalyx also showed a greater glycocalyx level in the LPX1 group than in the control (40.4 vs 36.3 arbitrary units). Additionally, LPX1 treated animals were able to sustain a higher mean arterial pressure (82 vs 45mmHg), and oxygen saturation throughout the resuscitation period measured at 15 and 30 minutes following LPX1 infusion (98.4% SpO2 vs. 99.0% SpO2 at 30 minutes resuscitation). Conclusions: Ferroptosis inhibitor LPX1 can reduce morbidity acutely during hemorrhagic shock and can protect the endothelial cell glycocalyx from oxidative damage due to its ability to slow the generation of reactive oxygen species and lipid hydroperoxides.

Nanoactuator for Neuronal Optoporation.

Light-driven modulation of neuronal activity at high spatial-temporal resolution is becoming of high interest in neuroscience. In addition to optogenetics, nongenetic membrane-targeted nanomachines that alter the electrical state of the neuronal membranes are in demand. Here, we engineered and characterized a photoswitchable conjugated compound (BV-1) that spontaneously partitions into the neuronal membrane and undergoes a charge transfer upon light stimulation. The activity of primary neurons is not affected in the dark, whereas millisecond light pulses of cyan light induce a progressive decrease in membrane resistance and an increase in inward current matched to a progressive depolarization and action potential firing. We found that illumination of BV-1 induces oxidation of membrane phospholipids, which is necessary for the electrophysiological effects and is associated with decreased membrane tension and increased membrane fluidity. Time-resolved atomic force microscopy and molecular dynamics simulations performed on planar lipid bilayers revealed that the underlying mechanism is a light-driven formation of pore-like structures across the plasma membrane. Such a phenomenon decreases membrane resistance and increases permeability to monovalent cations, namely, Na+, mimicking the effects of antifungal polyenes. The same effect on membrane resistance was also observed in nonexcitable cells. When sustained light stimulations are applied, neuronal swelling and death occur. The light-controlled pore-forming properties of BV-1 allow performing "on-demand" light-induced membrane poration to rapidly shift from cell-attached to perforated whole-cell patch-clamp configuration. Administration of BV-1 to ex vivo retinal explants or in vivo primary visual cortex elicited neuronal firing in response to short trains of light stimuli, followed by activity silencing upon prolonged light stimulations. BV-1 represents a versatile molecular nanomachine whose properties can be exploited to induce either photostimulation or space-specific cell death, depending on the pattern and duration of light stimulation.

Dihydroquercetin improves experimental acute liver failure by targeting ferroptosis and mitochondria-mediated apoptosis through the SIRT1/p53 axis

BackgroundFerroptosis and mitochondria-mediated apoptosis are both involved in the pathogenesis of acute liver failure (ALF). Ferroptosis-produced reactive oxygen species (ROS) trigger the chain oxidation of polyunsaturated phospholipids and promote mitochondrial apoptosis. Dihydroquercetin (DHQ) also plays an important protective role against liver injury. PurposeHere, we aimed to investigate the protective effects of DHQ on ALF. We also explored the underlying mechanism. MethodsWe established a Lipopolysaccharide (LPS)/D-galactosamine (D-Gal)-induced ALF mouse model and tumor necrosis factor-α (TNF-α)/D-Gal-induced ALF LO2 cell model. 2′,7′-Dichlorofluorescein diacetate (DCFH-DA) and Dihydroethidium (DHE) were used to detect total ROS levels. Lipid ROS was assessed using C11-BODIPY flow cytometry. Lipid peroxidative products levels were detected using MDA ELISA assay and 4-hydroxynonenal (4-HNE) immunohistochemistry. QRT-PCR and western blots were used to test mRNA and protein expression levels, respectively. Cell viability was evaluated with CCK8 assay, and apoptosis was analyzed using flow cytometry. ResultsDHQ treatment improved LPS/D-Gal-induced ALF, as well as TNF-α/D-Gal-induced reductions in LO2 viability and increased sirtuin 1 (SIRT1) expression. DHQ pretreatment also reduced the accumulation of ROS, reduced lipid peroxidation, elevated mitochondrial membrane potentials (ΔΨm), and decreased liver cell apoptosis both in vivo and in vitro. Additionally, the knockdown of SIRT1 and p53 activator (Tenovin-6) treatment reversed DHQ's inhibitory effects on ferroptosis and mitochondria-mediated apoptosis in vitro. DHQ enhanced p53 deacetylation by both up-regulating SIRT1 expression and directly bonding to SIRT1. We also found that Tenovin-6′s stimulatory effects on ferroptosis and mitochondria-mediated apoptosis in the DHQ-treated LO2 ALF cell model were partially attenuated by overexpression of solute carrier family 7member 11 (SLC7A11), as well as by apoptotic protease activating factor 1 (Apaf-1) knockdown. ConclusionOur results suggest that DHQ alleviated ALF by inhibiting both ferroptosis and mitochondria-mediated apoptosis by regulating the SIRT1/p53 axis. Thus, DHQ may serve as a novel therapy for ALF.

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3

Ferroptosis is a novel cell death mechanism that is mediated by iron-dependent lipid peroxidation. It may be involved in atherosclerosis development. Products of phospholipid oxidation play a key role in atherosclerosis. 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC) is a phospholipid oxidation product present in atherosclerotic lesions. It remains unclear whether PGPC causes atherosclerosis by inducing endothelial cell ferroptosis. In this study, human umbilical vein endothelial cells (HUVECs) were treated with PGPC. Intracellular levels of ferrous iron, lipid peroxidation, superoxide anions (O2•−), and glutathione were detected, and expression of fatty acid binding protein-3 (FABP3), glutathione peroxidase 4 (GPX4), and CD36 were measured. Additionally, the mitochondrial membrane potential (MMP) was determined. Aortas from C57BL6 mice were isolated for vasodilation testing. Results showed that PGPC increased ferrous iron levels, the production of lipid peroxidation and O2•−, and FABP3 expression. However, PGPC inhibited the expression of GPX4 and glutathione production and destroyed normal MMP. These effects were also blocked by ferrostatin-1, an inhibitor of ferroptosis. FABP3 silencing significantly reversed the effect of PGPC. Furthermore, PGPC stimulated CD36 expression. Conversely, CD36 silencing reversed the effects of PGPC, including PGPC-induced FABP3 expression. Importantly, E06, a direct inhibitor of the oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine IgM natural antibody, inhibited the effects of PGPC. Finally, PGPC impaired endothelium-dependent vasodilation, ferrostatin-1 or FABP3 inhibitors inhibited this impairment. Our data demonstrate that PGPC impairs endothelial function by inducing endothelial cell ferroptosis through the CD36 receptor to increase FABP3 expression. Our findings provide new insights into the mechanisms of atherosclerosis and a therapeutic target for atherosclerosis.

Oxidative Stress Induces Changes in Molecular Markers Associated with Ferroptosis in Human Spermatozoa.

Ferroptosis is a type of iron-dependent regulated cell death characterized by increased bioavailability of redox-active iron, loss of GPX4 antioxidant capacity, and oxidation of polyunsaturated fatty acid-containing phospholipids mediated by reactive oxygen species (ROS). The aim of this study was to evaluate the effect of oxidative stress induced by arachidonic acid (AA) on ferroptotic cell death in human spermatozoa. Spermatozoa from normozoospermic donors were exposed to AA (5, 25, and 50 µM) for 1 hour at 37 ℃, including an untreated control. Oxidative stress was confirmed by evaluation of cytosolic and mitochondrial ROS production, viability, mitochondrial membrane potential (ΔΨm) and motility. Subsequently, molecular markers of ferroptosis including iron content, levels of GPX4, SLC7A11, ACSL4, IREB2 and lipid peroxidation were evaluated. The analyses were carried out using either flow cytometry, a microplate reader or confocal laser microscopy. AA-induced oxidative stress showed increased cytosolic and mitochondrial ROS production accompanied by impairedΔΨm, viability and motility in human spermatozoa. These results were associated with biochemical and molecular markers related to ferroptotic cell death including an increase in iron content in the form of ferrous (Fe2+) ions, SLC7A11, ACSL4, IREB2, a decrease in the level of GPX4, and an increase in the level of lipid peroxidation compared to the untreated control. This study revealed that AA-induced oxidative stress induces cell death with biochemical characteristics of ferroptosis in human spermatozoa, demonstrating another mechanism of alteration of sperm function induced by oxidative stress and could establish new therapeutic objectives to prevent the decrease in sperm quality mediated by oxidative stress.

Preparation, characterization, and release properties of Rosa roxburghii Tratt seed oil and β-carotene-coloaded proliposomes.

Rosa roxburghii Tratt seed oil (RSO) and β-carotene (βC) were chosen to prepare proliposomes by the thin-film dispersion method. The characteristics of unloaded proliposome, RSO proliposome (L-R), βC proliposome (L-β), and RSO/βC proliposome (L-R-β) were analyzed, and their antioxidant activity, storage stability, and release properties were investigated. The proliposomes had an encapsulation efficiency (RSO, βC) higher than 83.10%, nanometer size, smooth surface, and irregular structure. L-R-β showed better dispersibility, stability, and antioxidant activity than L-R and L-β. Simultaneous encapsulation of RSO and βC reduced the phospholipid oxidation of proliposomes and improved the retention rate of RSO in storage environments of 4, 25, and 40°C. Moreover, the RSO and βC release kinetics of proliposomes in the simulated saliva fluid and gastric fluid phases can be described by the first-order model, and the Korsmeyr-Peppas method was applied to describe their release mechanism in the simulated intestinal fluid phase.

Lyophilization enhances the stability of Panax notoginseng total saponins-loaded transfersomes without adverse effects on ex vivo/in vivo skin permeation

Transfersomes (TFSs) have been extensively investigated to enhance transdermal drug delivery. As a colloidal dispersion system, TFSs are prone to problems such as particle aggregation and sedimentation, oxidation and decomposition of phospholipids. To enhance the stability of panax notoginseng saponins (PNS)-loaded transfersomes (PNS-TFSs) without adverse influences on their skin permeation, we prepared lyophilized PNS-loaded transfersomes (PNS-FD-TFSs), clarified their physicochemical characteristics and investigated their in vitro drug release, ex vivo skin permeation/deposition and in vivo pharmacokinetics. In this study, a simple, fast and controllable process was developed for preparing lyophilized PNS-TFSs. In the optimized PNS-FD-TFS formulation, sucrose and trehalose were added to the PNS-TFS dispersion with a mass ratio of trehalose, sucrose, and phospholipid of 3:2:1, and the mixture was frozen at −80 °C for 12 h followed by lyophilization at −45 °C and 5 Pa for 24 h. The optimized formulation of PNS-FD-TFSs was screened based on the appearance and reconstitution time of the lyophilized products, vesicle size, and PDI of the freshly reconstituted dispersions. It maintained stable physicochemical properties for at least 6 months at 4 °C. The vesicle size of PNS-FD-TFSs was below 100 nm and homogenous with a polydispersity index of 0.2 after reconstitution. The average encapsulation efficiencies of the five index saponins notoginsenoside R1 (NGR1), ginsenoside Rg1 (GRg1), ginsenoside Re (GRe), ginsenoside Rb1 (GRb1) and ginsenoside Rd (GRd) in PNS-FD-TFSs were 68.41 ± 5.77%, 68.95 ± 6.08%, 65.46 ± 10.95%, 91.50 ± 5.62% and 95.78 ± 1.70%, respectively. The reconstituted dispersions of PNS-FD-TFSs were similar to PNS-TFSs in in vitro release, ex vivo skin permeation, and deposition. The pharmacokinetic studies showed that, compared with the PNS liposomes (PNS-LPS), the PNS-FD-TFS-loaded drug could permeate through the skin and enter the blood rapidly. It can be concluded that the lyophilization process can effectively improve the stability of PNS-TFSs without compromising their transdermal absorption properties.

Effect of oxyresveratrol on the quality and membrane lipid metabolism of shiitake mushroom (Lentinus edodes) during storage.

The effect of oxyresveratrol on postharvest quality and membrane lipid metabolism of shiitake mushroom was investigated. The result exhibited that oxyresveratrol retarded browning, maintained firmness and alleviated occurrence of decay of shiitake mushroom. The oxidation and hydrolysis of membrane phospholipids were suppressed by oxyresveratrol treatment, which was associated with reduced LOX and PLD activities and increased SOD and CAT activities. The membrane lipidomics of shiitake mushroom was determined by LC-MS. 385 lipid species and 13 fatty acids in membrane lipids were identified by multiple reaction monitoring method. Compared with control group, the phospholipic acid and lysophospholipid reduced by 29.24% and 21.29% in oxyresveratrol-treated group, respectively, which alleviated hydrolysis of phospholipid. Meanwhile, oxyresveratrol maintained the unsaturation of fatty acids and alleviated oxidation of phospholipid. These results demonstrated that oxyresveratrol could play a dual role of inhibiting the oxidation and hydrolysis of phospholipids to mitigate cellular damage of shiitake mushroom.

The effect of lutein on the oxidation of egg yolk phospholipids in a liposome model

Egg yolk phospholipids (PLs) extracted by organic solvent are prone to oxidation, while they are quite stable in egg yolk. This study was to verify the decisive role of lutein (naturally present in egg yolk) on the oxidative stability of PLs by constructing liposome. The liposome samples were heated at 100 °C for 10 min, and then the oxidation products of the liposome samples were analyzed by 1H NMR and GC–MS. The results showed that the concentrations of most of the oxidation products in the PLs-liposomes sample were significantly higher than those in the PLs&lutein-liposomes sample. Therefore, lutein could protect egg yolk PLs from oxidation, thus inhibiting the formation of lipid-derived volatile compounds. As those lipid-derived volatile compounds are the key fatty note odorants, this study has confirmed that the removal of lutein is the determining factor in using egg yolk PLs as an ideal precursor of fatty note odorants.

Mechanism of salt effect on flavor formation in lightly-salted large yellow croaker by integrated multiple intelligent sensory and untargeted lipidomics analyses

Salt has a great influence on food flavor formation. In this study, electronic tongue and nose, gas chromatography-mass spectrometry, liquid chromatography-mass spectrometry, and lipid oxidation levels were used to investigate the influence of different NaCl concentrations on the flavor formation of lightly salted large yellow croaker. The results showed that salt improves the sensory characteristics of the product. Hexanal, 2,5-octanedione, octanal, 1-octen-3-ol, nonanal, and heptanal were key flavor compounds. Phospholipids containing 18-carbon fatty acids are major flavor precursor substances. The TBARS values in samples increase with the increase of salt levels significantly (p < 0.05). Products marinated in 6% NaCl showed the highest lipase activity. Thus, NaCl promotes the hydrolysis and oxidation of phospholipids by increasing lipase activity to produce key flavor substances. This study provides valuable insights into the effects of NaCl on flavor formation, which may help to regulate the flavor of salt-reduced food.

Lipidomic analysis of seminal plasma in work-up of varicocele-associated male infertility

Background. Approximately 50 % of cases of infertility in couples are attributable to male factor. One of the most common causes of male infertility is varicose dilation of pampiniform plexus veins in spermatic cord, or varicocele. However, the fact that only in 10-45 % of cases microsurgical subinguinal varicocelectomy leads to a spontaneous pregnancy in a couple urges further search for a diagnostic marker which would be able to predict the success of surgical treatment of varicocele preoperatively.Aim. To study the features of lipid profile of seminal plasma in patients with varicocele and to evaluate the possibility of using lipidomic analysis of seminal plasma for patient selection prior to surgical treatment for varicocele.Materials and methods. Fifty three patients from infertile couples with varicocele and altered seminal parameters aged 18 to 44 years underwent microsurgical varicocelectomy as described by Marmar. All patients were treated in one department. The control group included 24 healthy normozoospermic men without varicocele who had proven fertility. The material for the study was the seminal plasma of men, lipid composition of which was determined by mass spectrometry.Results. No significant differences were found in lipid profiles of seminal plasma from men in control group and varicocele group, as well as in lipid profiles of seminal plasma obtained before and after surgery in same patients. Comparison of lipid profiles of seminal plasma provided by patients before microsurgical varicocelectomy, who had clinical effect (n = 15) and who did not have clinical effect (n = 16), revealed differences in level of HexCer-NDS d20:0/18:0 in the positive ion test and in levels of 8 other lipids in the negative ion test. These lipids are related to the oxidation of phospholipids, cardiolipins and phosphatidylethanolamines.Conclusion. The lipid profile of seminal plasma of patients who had clinical response to varicocele surgery is significantly different from the lipid profile of seminal plasma of non-responder patients.

Multi-omics analyses based on genes associated with oxidative stress and phospholipid metabolism revealed the intrinsic molecular characteristics of pancreatic cancer

Oxidative stress (OS), which impacts lipid metabolic reprogramming, can affect the biological activities of cancer cells. How oxidative stress and phospholipid metabolism (OSPM) influence the prognosis of pancreatic cancer (PC) needs to be elucidated. The metabolic data of 35 pancreatic tumor samples, 34 para-carcinoma samples, and 31 normal pancreatic tissues were obtained from the previously published literature. Pan-cancer samples were obtained from The Cancer Genome Atlas (TCGA). And the Gene Expression Omnibus (GEO), International Cancer Genome Consortium (ICGC), ArrayExpress, and the Genotype-Tissue Expression (GTEx) databases were searched for more PC and normal pancreatic samples. The metabolites in PC were compared with normal and para-carcinoma tissues. The characteristics of the key OSPM genes were summarized in pan-cancer. The random survival forest analysis and multivariate Cox regression analysis were utilized to construct an OSPM-related signature. Based on this signature, PC samples were divided into high- and low-risk subgroups. The dysregulations of the tumor immune microenvironment were further investigated. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was conducted to investigate the expression of genes in the signature in PC and normal tissues. The protein levels of these genes were further demonstrated. In PC, metabolomic studies revealed the alteration of PM, while transcriptomic studies showed different expressions of OSPM-related genes. Then 930 PC samples were divided into three subtypes with different prognoses, and an OSPM-related signature including eight OSPM-related genes (i.e., SLC2A1, MMP14, TOP2A, MBOAT2, ANLN, ECT2, SLC22A3, and FGD6) was developed. High- and low-risk subgroups divided by the signature showed different prognoses, expression levels of immune checkpoint genes, immune cell infiltration, and tumor microenvironment. The risk score was negatively correlated with the proportion of TIL, pDC, Mast cell, and T cell co-stimulation. The expression levels of genes in the signature were verified in PC and normal samples. The protein levels of SLC2A1, MMP14, TOP2A, MBOAT2, ANLN, and SLC22A3 showed up-regulation in PC samples compared with normal tissues. After integrating metabolomics and transcriptomics data, the alterations in OSPM in PC were investigated, and an OSPM-related signature was developed, which was helpful for the prognostic assessment and individualized treatment for PC.