Formation Of Lipid Oxidation Products Research Articles

Mathematical Modeling of Alpha-Tocopherol Early Degradation Kinetics to Predict the Shelf-Life of Bulk Oils.

The kinetics of lipid oxidation includes a lag phase followed by an exponential increase in oxidation products, which cause rancidity. Current models focus on the slope of this exponential curve for shelf-life estimation, which still requires the measurement of full oxidation kinetics. In this paper, we analyzed the formation of lipid oxidation products in stripped soybean oil containing different levels of α-tocopherol. The lag phases of lipid hydroperoxides and headspace hexanal formation were found to have a strong positive correlation with the α-tocopherol depletion time. We propose that the kinetics of antioxidant (α-tocopherol) depletion occur during the lag phase and could serve as an early shelf-life indicator. Our results showed that α-tocopherol degradation can be described by Weibull kinetics over a wide range of initial concentrations. Furthermore, we conducted in silico investigations using Monte Carlo simulations to critically evaluate the feasibility and sensitivity of the shelf-life prediction using early antioxidant degradation kinetics. Our results revealed that the shelf life of soybean oil may be accurately predicted as early as 20% of the overall shelf life. This innovative approach provides a more efficient and faster assessment of shelf life, ultimately reducing waste and enhancing product quality.

Alcoholic beverages reduce oxidation during in vitro gastrointestinal digestion of meat and fish, but induce fatty acid ethyl ester formation

The effect of selected phenolic-containing beers (pale lager, barley wine, tripel), white wine, and red wine on the formation of lipid oxidation products (thiobarbituric acid reactive substances, 4-hydroxy-2-hexenal, 4-hydroxy-2-nonenal) and protein carbonylation during simulated gastrointestinal digestion of pork and salmon was investigated. Greater antioxidant effects of the beverages were observed during the digestion of salmon, whereas antioxidant effects were less pronounced or absent during the digestion of pork. Red wine contained the highest levels of phenolics, accompanied by the highest antioxidant effects among the beverages tested. Secondly, the simultaneous formation of potentially harmful fatty acid ethyl esters (FAEEs) was observed for the first time when these muscle foods were digested with the beers and wines tested, or with pure ethanol. These FAEEs were formed by lipase activity in the presence of ethanol, which was blocked by the lipase inhibitor orlistat. The formation of selected FAEEs corresponded well with the levels of their precursor fatty acids in muscle, resulting in different FAEE profiles in the digests of chicken, pork, beef, or salmon with ethanol. In conclusion, the formation of potentially harmful FAEE may counteract the observed beneficial antioxidant effects of phenolic-rich alcoholic beverages during the gastrointestinal digestion of muscle foods.

Replacement of soybean oil by Hermetia illucens larvae fat in broiler diets alters the breast muscle lipidome and reduces lipid oxidation of the breast muscle during heat-processing

ABSTRACT Replacement of soybean oil by insect fat from Hermetia illucens (HI) has been reported to increase the proportions of saturated fatty acids (SFA) and decrease those of polyunsaturated fatty acids (PUFA) in total lipids of breast and thigh meat in broilers. Since the susceptibility of meat to oxidation is strongly dependent on its PUFA content, the present study hypothesised that replacement of soybean oil by HI larvae fat in broiler diets reduces the formation of lipid oxidation products, including oxidation products of cholesterol and phytosterols, in heat-processed breast muscle of broilers. To test this hypothesis, 100 male, 1-day-old Cobb 500 broilers were assigned to three groups and fed three different nutrient adequate diets, which varied only in the fat source (group HI-0: 0% HI larvae fat and 5% soybean oil; group HI-2.5: 2.5% HI larvae fat and 2.5% soybean oil; group HI-5.0: 5.0% HI larvae fat and 0% soybean oil), in a three-phase feeding system for 35 days. While the growth performance of the broilers was not different, the absolute and relative breast muscle weights were higher in group HI-5.0 than in group HI-0 (p < 0.05). The proportions of C12:0, C14:0, C14:1, C16:0, C16:1 and total SFA were higher and those of C18:1, C18:2 n-6, C18:3 n-3 and total PUFA were lower in breast muscle total lipids of group HI-5.0 than in groups HI-2.5 and HI-0 (p < 0.05). Lipidomic analysis of breast muscle revealed that the concentration of triacylglycerols was 46% and 53% lower in groups HI-2.5 and HI-5.0, respectively, than in group HI-0 (p < 0.05), whereas all other lipid classes detected did not differ among groups. Concentrations of thiobarbituric acid-reactive substances, 7α-hydroxycholesterol, 7β-hydroxycholesterol and total cholesterol oxidation products in heat-processed breast muscle were lower in group HI-5.0 than in group HI-0 (p < 0.05). Concentrations of oxidation products of phytosterols in heat-processed breast muscle were generally much lower than those of cholesterol oxidation products and did not differ between the three groups of broilers. In conclusion, complete replacement of soybean oil with HI larvae fat in broiler diets strongly alters the fatty acid composition of breast muscle total lipids and reduce lipid oxidation of the breast muscle during heat-processing.

Characterization of the aroma profile of quinoa (Chenopodium quinoa Willd.) and assessment of the impact of malting on the odor-active volatile composition.

Quinoa (Chenopodium quinoa Willd.) is a gluten-free pseudocereal, rich in starch and high-quality proteins. It can be used as a cereal. Recently, a variety of nontraditional food products were developed; however, the sharp bitterness and the earthy aroma of unprocessed quinoa interfered with the acceptance of these products. Malting of cereals is known to improve their processing properties and enhance their sensory quality. To evaluate the acceptance and potential of quinoa malt as a raw material for beverage production, malt quality indicators (e.g., soluble protein) and the aroma profiles of different quinoa malts were compared. Initial sensory assessment of quinoa in its native and malted state identified differences in their aroma profiles and revealed that pleasant nutty and caramel aromas were formed by malting. Subsequently, three complementary isolation techniques and gas chromatography-olfactometry/mass spectrometry (GC-O/MS) were used for volatile analysis. Instrumental analysis detected 34 and 62 odor-active regions in native quinoa and quinoa malt, respectively. In the second part, storage and the impact of three malting parameters on volatile formation were examined. By varying the malting parameters, seven additional odor-active malting byproducts were revealed. Three naturally occurring methoxypyrazines were identified as important contributors to the characteristic quinoa aroma. In all fresh quinoa malts a similar number of volatile compounds was perceived but their intensity and composition varied. Higher germination temperature promoted the formation of lipid oxidation products. Fatty smelling compounds and carboxylic acids, formed during storage, were classified as aging indicators of quinoa malt. © 2022 The Authors. Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Synthesized alkyl ferulates with different chain lengths inhibited the formation of lipid oxidation products in soybean oil during deep frying

The hydrophilic nature of ferulic acid limits its applications under lipophilic conditions. This study set out to evaluate the antioxidant efficacy of alkyl ferulates with different chain lengths in soybean oil under frying conditions. Ferulic acid was esterified with four unbranched fatty alcohols (C4:0-C16:0), and tert-butylhydroquinone (TBHQ) served as a standard for comparison. The antioxidant effect of alkyl ferulates increased with the alkyl chain length. The addition of antioxidants could inhibit increases in the levels of p-anisidine, total polar compounds, conjugated dienes, conjugated trienes, oxidized triglyceride monomers, triglyceride dimers, triglyceride oligomers, and glycerol core aldehydes efficiently, and the inhibitory effects of hexadecyl ferulate was the strongest. Moreover, hexadecyl ferulate and TBHQ exhibited better inhibitory effects on the generation of n-alkanals, (E)-2-alkenals, and 4-oxo-alkanals determined by 1H nuclear magnetic resonance than others. Hence, the long-chain alkyl ferulates meet the industrial demands for ideal antioxidants with strong antioxidant capacity at high temperatures.

TRPV1 as an anti-ferroptotic target in osteoarthritis.

Osteoarthritis (OA) is the most common joint disease worldwide and considered as uncurable, which is mainly attributed to its complex pathophysiology, affecting the whole joint. Progressive cartilage degeneration represents the most prominent hallmark of OA. This degeneration is driven by various pathomechanisms, comprising cell death, oxidative stress, and excessive catabolism.1Riegger J. Joos H. Palm H.-G. et al.Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine.Osteoarthrit Cartil. 2016; 24: 2171-2180Summary Full Text Full Text PDF PubMed Scopus (20) Google Scholar,2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar Because of its exceptional hypocellularity, chondrocyte death has detrimental consequences on cartilage. Various forms of programmed cell death, based on different underlying mechanisms, have been identified in OA cartilage during the last years. However, oxidative stress might play a crucial role in all forms.1Riegger J. Joos H. Palm H.-G. et al.Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine.Osteoarthrit Cartil. 2016; 24: 2171-2180Summary Full Text Full Text PDF PubMed Scopus (20) Google Scholar,2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar In contrast to non-lytic apoptotic cell death, which is considered as a clean way to eliminate damaged cells, necroptosis and pyroptosis are highly pro-inflammatory due to membrane rupture and subsequent release of intracellular components.2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar,3Yang J. Hu S. Bian Y. et al.Targeting cell death: pyroptosis, ferroptosis, apoptosis and necroptosis in osteoarthritis.Front Cell Dev Biol. 2021; 9789948Google Scholar Taken together, not only the fact that chondrocytes undergo programmed cell death, but also the “how”, might have a decisive impact on disease progression and has thus become a hot topic in OA research.One decade ago, Dixon et al. first proposed a new form of programmed cell death, namely iron-dependent ferroptosis, which is mainly characterized by lipid peroxidation.4Dixon S.J. Lemberg K.M. Lamprecht M.R. et al.Ferroptosis: an iron-dependent form of nonapoptotic cell death.Cell. 2012; 149: 1060-1072Summary Full Text Full Text PDF PubMed Scopus (4784) Google Scholar By the interaction with reactive oxygen species, free iron can promote the formation of lipid oxidation products. The lipid repair enzyme glutathione peroxidase 4 (GPX4) requires glutathione to convert cytotoxic lipid hydroperoxides into a non-toxic form, a crucial mechanism to prevent ferroptosis. Direct inhibition of GPX4 activity or impairment of cysteine uptake and subsequent glutathione depletion results in accumulation of lipid peroxides and thus initiates ferroptosis.5Yang W.S. Kim K.J. Gaschler M.M. et al.Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis.Proc Natl Acad Sci U S A. 2016; 113: E4966-E4975Crossref PubMed Scopus (732) Google ScholarDespite previous reports of ferroptotic cell death in murine OA models, first evidence for iron-induced chondrocyte death in human OA was only given in 2022. Mioa et al. described iron accumulation in synovial fluid and degenerated cartilage from OA patients and confirmed concurrent reduction in GPX4 levels and enhanced ferroptosis.6Miao Y. Chen Y. Xue F. et al.Contribution of ferroptosis and GPX4’s dual functions to osteoarthritis progression.EBioMedicine. 2022; 76103847Summary Full Text Full Text PDF PubMed Scopus (16) Google Scholar A few months later, Lv and colleagues shed further light on the underlying mechanisms of ferroptosis in chondrocytes, as recently published in eBioMedicine.7Lv Z. Han J. Li J. et al.Single cell RNA-seq analysis identifies ferroptotic chondrocyte cluster and reveals TRPV1 as an anti-ferroptotic target in osteoarthritis.eBioMedicine. 2022; 84104258Summary Full Text Full Text PDF Scopus (1) Google Scholar By means of a single cell RNA sequencing on human OA cartilage, they determined the molecular signature of a ferroptotic chondrocyte cluster, which was distinguished by genes involved in oxidative stress, lipid oxidation, Fe2+ response, and ferroptosis, while markers associated with other modalities of cell death were hardly detectable. Considering the lack of distinct biomarkers or criteria to determine ferroptotic chondrocytes, this finding is of high relevance. Moreover, the authors identified transient receptor potential vanilloid 1 (TRPV1) channel as a potential anti-ferroptotic target. In fact, TRPV1 was substantially downregulated during the progression of OA as demonstrated in human cartilage and a murine injury-induced OA model. Lv and colleagues confirmed that activation of TRPV1 by capsaicin (CPS) significantly protected isolated chondrocytes from chemically induced ferroptosis in vitro, while pharmacological inhibition or siRNA-mediated silencing of TRPV1 impaired the cell protection. Intra-articular injection of CPS not only prevented chondrocyte ferroptosis but also preserved the expression of TRPV1 in injury-induced OA. The anti-ferroptotic effects were attributed to the enhanced expression of GPX4 as a downstream target of TRPV1, which was confirmed in human cartilage and the murine OA model. Interestingly, another mechanosensitive ion channel, namely Piezo 1, was previously associated with chondrocyte ferroptosis. In contrast to TRPV1, Piezo 1 activation upon mechanical overload and subsequent calcium influx increased ferroptosis, while the inhibition of the ion channel increased GPX4 expression and reduced ferroptosis.8Wang S. Li W. Zhang P. et al.Mechanical overloading induces GPX4-regulated chondrocyte ferroptosis in osteoarthritis via Piezo1 channel facilitated calcium influx.J Adv Res. 2022; Crossref Scopus (2) Google ScholarIn accordance to previous reports, Lv and colleagues demonstrated that prevention of ferroptosis leads to chondroprotection, which might result from attenuated release of pro-inflammatory mediators due to reduced cell lysis, but also the upregulation of GPX4, which has additionally been described as negative regulator of the catabolic MAPK/NF-kB pathway.6Miao Y. Chen Y. Xue F. et al.Contribution of ferroptosis and GPX4’s dual functions to osteoarthritis progression.EBioMedicine. 2022; 76103847Summary Full Text Full Text PDF PubMed Scopus (16) Google Scholar Moreover, the authors discussed the reduced cartilage destruction and attenuated synovitis upon CPS-mediated TRPV1 activation by the potential inhibition of M1 macrophage polarization, as recently described in a rat OA model.9Lv Z. Xu X. Sun Z. et al.TRPV1 alleviates osteoarthritis by inhibiting M1 macrophage polarization via Ca(2+)/CaMKII/Nrf2 signaling pathway.Cell Death Dis. 2021; 12: 504Crossref PubMed Scopus (20) Google ScholarOverall, Lv and colleagues not only underline the essential role of GPX4 in preventing ferroptosis and cartilage degeneration, but also provide a new therapeutic target to promote GPX4 expression, namely TRPV1. However, it should be considered hat TRPV1 sensitization was found to be involved in chronic joint pain, implying that intra-articular application of agonists might exacerbate pain in OA.10Kelly S. Chapman R.J. Woodhams S. et al.Increased function of pronociceptive TRPV1 at the level of the joint in a rat model of osteoarthritis pain.Ann Rheum Dis. 2015; 74: 252-259Crossref PubMed Scopus (72) Google Scholar In view of these controversial results concerning the role of TRPV1, further studies are needed. Nevertheless, it is indisputable that programmed cell death substantially contributes to OA progression and thus represents a relevant therapeutic target. When addressing chondrocyte death, it should be kept in mind that inhibition of one mode of cell death might promote a shift towards a different, potentially more detrimental, pathway.2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar And in the end, programmed elimination of damaged chondrocytes might to some extent be beneficial regarding the maintenance of the tissue homeostasis by preventing accumulation of dysfunctional cells.ContributorJ.R. designed and wrote the present commentary solely. Osteoarthritis (OA) is the most common joint disease worldwide and considered as uncurable, which is mainly attributed to its complex pathophysiology, affecting the whole joint. Progressive cartilage degeneration represents the most prominent hallmark of OA. This degeneration is driven by various pathomechanisms, comprising cell death, oxidative stress, and excessive catabolism.1Riegger J. Joos H. Palm H.-G. et al.Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine.Osteoarthrit Cartil. 2016; 24: 2171-2180Summary Full Text Full Text PDF PubMed Scopus (20) Google Scholar,2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar Because of its exceptional hypocellularity, chondrocyte death has detrimental consequences on cartilage. Various forms of programmed cell death, based on different underlying mechanisms, have been identified in OA cartilage during the last years. However, oxidative stress might play a crucial role in all forms.1Riegger J. Joos H. Palm H.-G. et al.Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine.Osteoarthrit Cartil. 2016; 24: 2171-2180Summary Full Text Full Text PDF PubMed Scopus (20) Google Scholar,2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar In contrast to non-lytic apoptotic cell death, which is considered as a clean way to eliminate damaged cells, necroptosis and pyroptosis are highly pro-inflammatory due to membrane rupture and subsequent release of intracellular components.2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar,3Yang J. Hu S. Bian Y. et al.Targeting cell death: pyroptosis, ferroptosis, apoptosis and necroptosis in osteoarthritis.Front Cell Dev Biol. 2021; 9789948Google Scholar Taken together, not only the fact that chondrocytes undergo programmed cell death, but also the “how”, might have a decisive impact on disease progression and has thus become a hot topic in OA research. One decade ago, Dixon et al. first proposed a new form of programmed cell death, namely iron-dependent ferroptosis, which is mainly characterized by lipid peroxidation.4Dixon S.J. Lemberg K.M. Lamprecht M.R. et al.Ferroptosis: an iron-dependent form of nonapoptotic cell death.Cell. 2012; 149: 1060-1072Summary Full Text Full Text PDF PubMed Scopus (4784) Google Scholar By the interaction with reactive oxygen species, free iron can promote the formation of lipid oxidation products. The lipid repair enzyme glutathione peroxidase 4 (GPX4) requires glutathione to convert cytotoxic lipid hydroperoxides into a non-toxic form, a crucial mechanism to prevent ferroptosis. Direct inhibition of GPX4 activity or impairment of cysteine uptake and subsequent glutathione depletion results in accumulation of lipid peroxides and thus initiates ferroptosis.5Yang W.S. Kim K.J. Gaschler M.M. et al.Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis.Proc Natl Acad Sci U S A. 2016; 113: E4966-E4975Crossref PubMed Scopus (732) Google Scholar Despite previous reports of ferroptotic cell death in murine OA models, first evidence for iron-induced chondrocyte death in human OA was only given in 2022. Mioa et al. described iron accumulation in synovial fluid and degenerated cartilage from OA patients and confirmed concurrent reduction in GPX4 levels and enhanced ferroptosis.6Miao Y. Chen Y. Xue F. et al.Contribution of ferroptosis and GPX4’s dual functions to osteoarthritis progression.EBioMedicine. 2022; 76103847Summary Full Text Full Text PDF PubMed Scopus (16) Google Scholar A few months later, Lv and colleagues shed further light on the underlying mechanisms of ferroptosis in chondrocytes, as recently published in eBioMedicine.7Lv Z. Han J. Li J. et al.Single cell RNA-seq analysis identifies ferroptotic chondrocyte cluster and reveals TRPV1 as an anti-ferroptotic target in osteoarthritis.eBioMedicine. 2022; 84104258Summary Full Text Full Text PDF Scopus (1) Google Scholar By means of a single cell RNA sequencing on human OA cartilage, they determined the molecular signature of a ferroptotic chondrocyte cluster, which was distinguished by genes involved in oxidative stress, lipid oxidation, Fe2+ response, and ferroptosis, while markers associated with other modalities of cell death were hardly detectable. Considering the lack of distinct biomarkers or criteria to determine ferroptotic chondrocytes, this finding is of high relevance. Moreover, the authors identified transient receptor potential vanilloid 1 (TRPV1) channel as a potential anti-ferroptotic target. In fact, TRPV1 was substantially downregulated during the progression of OA as demonstrated in human cartilage and a murine injury-induced OA model. Lv and colleagues confirmed that activation of TRPV1 by capsaicin (CPS) significantly protected isolated chondrocytes from chemically induced ferroptosis in vitro, while pharmacological inhibition or siRNA-mediated silencing of TRPV1 impaired the cell protection. Intra-articular injection of CPS not only prevented chondrocyte ferroptosis but also preserved the expression of TRPV1 in injury-induced OA. The anti-ferroptotic effects were attributed to the enhanced expression of GPX4 as a downstream target of TRPV1, which was confirmed in human cartilage and the murine OA model. Interestingly, another mechanosensitive ion channel, namely Piezo 1, was previously associated with chondrocyte ferroptosis. In contrast to TRPV1, Piezo 1 activation upon mechanical overload and subsequent calcium influx increased ferroptosis, while the inhibition of the ion channel increased GPX4 expression and reduced ferroptosis.8Wang S. Li W. Zhang P. et al.Mechanical overloading induces GPX4-regulated chondrocyte ferroptosis in osteoarthritis via Piezo1 channel facilitated calcium influx.J Adv Res. 2022; Crossref Scopus (2) Google Scholar In accordance to previous reports, Lv and colleagues demonstrated that prevention of ferroptosis leads to chondroprotection, which might result from attenuated release of pro-inflammatory mediators due to reduced cell lysis, but also the upregulation of GPX4, which has additionally been described as negative regulator of the catabolic MAPK/NF-kB pathway.6Miao Y. Chen Y. Xue F. et al.Contribution of ferroptosis and GPX4’s dual functions to osteoarthritis progression.EBioMedicine. 2022; 76103847Summary Full Text Full Text PDF PubMed Scopus (16) Google Scholar Moreover, the authors discussed the reduced cartilage destruction and attenuated synovitis upon CPS-mediated TRPV1 activation by the potential inhibition of M1 macrophage polarization, as recently described in a rat OA model.9Lv Z. Xu X. Sun Z. et al.TRPV1 alleviates osteoarthritis by inhibiting M1 macrophage polarization via Ca(2+)/CaMKII/Nrf2 signaling pathway.Cell Death Dis. 2021; 12: 504Crossref PubMed Scopus (20) Google Scholar Overall, Lv and colleagues not only underline the essential role of GPX4 in preventing ferroptosis and cartilage degeneration, but also provide a new therapeutic target to promote GPX4 expression, namely TRPV1. However, it should be considered hat TRPV1 sensitization was found to be involved in chronic joint pain, implying that intra-articular application of agonists might exacerbate pain in OA.10Kelly S. Chapman R.J. Woodhams S. et al.Increased function of pronociceptive TRPV1 at the level of the joint in a rat model of osteoarthritis pain.Ann Rheum Dis. 2015; 74: 252-259Crossref PubMed Scopus (72) Google Scholar In view of these controversial results concerning the role of TRPV1, further studies are needed. Nevertheless, it is indisputable that programmed cell death substantially contributes to OA progression and thus represents a relevant therapeutic target. When addressing chondrocyte death, it should be kept in mind that inhibition of one mode of cell death might promote a shift towards a different, potentially more detrimental, pathway.2Riegger J. Brenner R.E. Evidence of necroptosis in osteoarthritic disease: investigation of blunt mechanical impact as possible trigger in regulated necrosis.Cell Death Dis. 2019; 10: 683Crossref PubMed Scopus (28) Google Scholar And in the end, programmed elimination of damaged chondrocytes might to some extent be beneficial regarding the maintenance of the tissue homeostasis by preventing accumulation of dysfunctional cells. ContributorJ.R. designed and wrote the present commentary solely. J.R. designed and wrote the present commentary solely. None to declare. This work was supported by the European Social Fund and by the Ministry of Science, Research and Arts Baden-Wuerttemberg. Single cell RNA-seq analysis identifies ferroptotic chondrocyte cluster and reveals TRPV1 as an anti-ferroptotic target in osteoarthritisTRPV1 activation protects chondrocytes from ferroptosis and ameliorates OA progression by upregulating GPX4. Full-Text PDF Open Access

Regulation of lipid peroxidation in mitochondria by nitroglycerine

The mechanisms of lipid oxidation under the application of nitroglycerine (NG) were studied in isolated rat heart and liver mitochondria. Dose-dependent formation of diene conjugates (DC), leukotriene C4 (LTC4) and thromboxane B2 (TxB2) was shown. To disclose the mechanisms regulating lipid peroxidation in mitochondria, we studied the effect of NG application on the formation of prooxidants (H2O2 and free Fe2+), as well as xanthine oxidase and mtNOS activity as main sources of ROS and RNS. Based on the correlation dependences, we have found that DC, LTC4, and TxB2 formation was strongly dependent on hydroperoxide production and free divalent iron release in mitochondria. Also, DC formation exhibited the dependence on Ca2+ uptake in mitochondria. No dependence of lipid oxidation on xanthine oxidase activity was found. In heart, but not liver mitochondria, DC, LTC4, and TxB2 exhibited strong dependence on mtNOS activity, but were independent of nitrosothiols formation. This indicated that lipid oxidation was independent of direct protein nitrosylation caused by NG application. No dependence of lipid oxidation on mtNOS activity in liver was found, which agreed with much higher mtNOS activity in heart mitochondria, and suppression of mtNOS activity in liver mitochondria at high doses of NG. So, we came to the conclusion that under NG application ROS overproduction and free Fe2+ release promoted both enzymatic and non-enzymatic lipid oxidation in heart and liver mitochondria. Also, we hypothesized that RNS overproduction due to the elevated mtNOS activity in the heart could largely contribute to lipid peroxidation and promote much faster increase in the formation of lipid oxidation products in heart as compared to liver mitochondria, especially at high doses of NG. Obtained correlation dependences allowed us disclose free iron, hydroperoxide, and mtNOS activity as principal factors affecting lipid peroxidation in mitochondria under NG application.

Impact of Heating Temperature and Fatty Acid Type on the Formation of Lipid Oxidation Products During Thermal Processing.

Thermal treatment of lipids rich in fatty acids contributes to the formation of lipid oxidation products (LOPs), which have potentially harmful effects on human health. This study included soybean oil (SO), palm oil (PO), olive oil (OO), and lard oil (LO) as the research objects, with an aim to investigate the impact of heating temperature and fatty acid type on the generation of LOPs (α-dicarbonyl compounds, malondialdehyde (MDA), α,β-unsaturated aldehydes, and 16 volatile aldehydes). Results showed that LOPs increased significantly (p < 0.05) with the increase in temperature (100 ~ 200°C). Furthermore, the amount of 2,3-butanedione (159.53 μg/g), MDA (3.15 μg/g), 4-hydroxy-hexenal (3.03 μg/g), 2-butenal (292.18%), 2-pentenal (102.26%), hexanal (898.72%), and 2,4-heptadienal (E, E) (2182.05%) were more at 200°C in SO rich in polyunsaturated fatty acids (PUFAs) than other oils. Results from heat map analysis indicated that the 2, 4-heptadienal, and glyoxal related to the myristic acid of oil. Moreover, the MDA was in close association with PUFAs. Based on the effect of temperature and fatty acid type on the generation of LOPs, this study could serve as a control method to reduce harmful LOPs.

Physical and oxidative stability of food emulsions prepared with pea protein fractions

There is a growing interest in replacing dairy proteins with their plant-based counterparts in food emulsions. Plant proteins generally contain a substantial insoluble protein fraction, of which the properties may differ from the soluble proteins. Therefore, the use of a commercial pea protein isolate, its insoluble fraction and whey protein isolate to stabilize oil-in-water (O/W) emulsions is explored.In 100 g/kg O/W emulsions, the use of full pea protein isolate led to physically instable emulsions that showed droplet flocculation and coalescence, whereas its insoluble fraction and whey protein formed physically stable emulsions. The insoluble pea protein fraction was also able to physically stabilize high internal phase O/W emulsions (HIPEs) containing 700 g/kg oil, giving ~10 times higher viscosity than whey protein-based HIPEs.Under oxidative conditions, whey protein-stabilized emulsions showed extensive coalescence, and fast formation of lipid oxidation products. Insoluble pea protein-stabilized emulsions, showed fast lipid oxidation, but this did not affect the physical stability. In contrast, full pea proteins-based emulsions were physically instable in oxidative conditions but showed the lowest accumulation of oxidation products. These results suggest that the constituents of commercial pea protein isolate have specific functionalities, which is important knowledge for the design of stable plant protein-based emulsions.

Quercetin Inhibited the Formation of Lipid Oxidation Products in Thermally Treated Soybean Oil by Trapping Intermediates.

In this research, we studied the inhibitory mechanism of quercetin, one popular phenolic compound, against aldehyde formation in thermally treated soybean oil. It was found that quercetin reduced unsaturated aldehyde formation significantly, with the inhibitory effect decreased with the extension of the heating time. Meanwhile, quercetin had minimum effects on the fatty acid profile compared to untreated samples. Some new phenolic derivatives were formed in thermally treated soybean oil with quercetin, further analyzed by liquid chromatography-tandem mass spectrometry, and compared to newly synthesized derivatives (characterized by mass spectrometry and nuclear magnetic resonance spectroscopy). On the basis of their chemical structures, we proposed that quercetin reacted with 13-oxo-octadecadienoic acid, 10-oxo-hexadecenoic acid, and 10-oxo-octadecenoic acid formed from peroxidation of linoleic acid, palmitoleic acid, and oleic acid, respectively, to inhibit aldehyde formation. In addition, newly formed quercetin-3-O-hexanoate, quercetin-3-O-heptanoate, and quercetin-3-O-nonanoate showed weaker 2,2-diphenyl-1-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt radical cation scavenging activity and weaker antioxidant activity in soybean oil, which explained the decreased inhibitory activity of quercetin against aldehyde formation during heat treatment. More interesting, quercetin-3-O-hexanoate showed improved cellular antioxidant activity compared to the parent quercetin. Overall, quercetin inhibited the formation of lipid oxidation products in thermally treated soybean oil by reacting with early intermediates in the lipid oxidation reaction, and quercetin derivatives formed in the process could be with enhanced cellular antioxidant activity. Our results provide novel insight into the inhibitory mechanism of quercetin against the formation of lipid oxidation products.

Changes in Volatile Compound Profiles in Cold-Pressed Oils Obtained from Various Seeds during Accelerated Storage.

Cold-pressed oils are highly valuable sources of unsaturated fatty acids which are prone to oxidation processes, resulting in the formation of lipid oxidation products, which may deteriorate the sensory quality of the produced oil. The aim of the study was to determine the main volatile compounds which differentiate examined oils and could be used as the markers of lipid oxidation in various oils. In the experiment, cold-pressed oils—brown flaxseed, golden flaxseed, hempseed, milk thistle, black cumin, pumpkin, white poppy seed, blue poppy seed, white sesame, black sesame and argan oils from raw and roasted kernels—were analyzed. To induce oxidative changes, an accelerate storage test was performed, and oils were kept at 60 °C for 0, 2, 4, 7 and 10 days. Volatile compound profiling was performed using SPME-GC-HRToFMS. Additionally, basic measurements such as fatty acid composition, peroxide value, scavenging activity and phenolic compound contents were carried out. Multivariate statistical analyses with volatile compound profiling allow us to differentiate oils in terms of plant variety, oxidation level and seed treatment before pressing. Comparing black cumin cold-pressed oil with other oils, significant differences in volatile compound profiles and scavenging activity were observed. Compounds that may serve as indicators of undergoing oxidation processes in flaxseed, poppy seed, milk thistle and hemp oils were determined.

Lipid oxidation and aldehyde formation during in vitro gastrointestinal digestion of roasted scallop (Patinopecten yessoensis) - the role of added antioxidant of bamboo leaves.

This study investigated lipid oxidation and aldehyde formation in roasted scallop during in vitro gastrointestinal digestion, and the effects of co-digestion of antioxidant of bamboo leaves (AOB) on this process. The results showed that the contents of lipid hydroperoxides (LOOH), conjugated dienes (CD), and Schiff bases (SB) were increased during gastrointestinal digestion. Besides, malondialdehyde (MDA) levels and total aldehyde formation decreased initially at the gastric stage but increased at the intestinal stage. The results of HPLC-ESI-MS/MS analysis showed that the contents of hexanal (HEX), trans, trans-2,4-octadienal (ODE), trans, trans-2,4-decadienal (DDE), 4-hydroxyhexenal (HHE) and 4-hydroxynonenal (HNE) in the digestive juices were all initially decreased and then increased during gastrointestinal digestion. Meanwhile, the content of acrolein, propanal, and trans-2-pentenal at the end of intestinal digestion was lower than that in the initial stage of gastric digestion. Additionally, the digestion of roasted scallop caused significant oxidation of polyunsaturated fatty acids (PUFAs) and release of free fatty acids (FFA) in the intestinal phase, which were positively related to aldehyde production. However, co-digestion of AOB significantly reduced lipid oxidation and formation of lipid oxidation products (LOOH, CD, SB, and aldehyde) during gastrointestinal digestion, indicating that the addition of AOB was effective in reducing gastrointestinal lipid oxidation.

Effects of pectin and tomato paste as a natural antioxidant on inhibition of lipid oxidation and production of functional chicken breast sausage

In this study antioxidant effects of pectin and tomato paste (TP) on lipid oxidation and production of functional chicken breast sausage during refrigerated storage for 14 days were evaluated. Raw chicken sausage samples were enriched with different levels of TP containing 0, 1, 2 and 10% and 1% pectin, and peroxide value (PV), thiobarbituric acid reactive substances (TBARS) and sensory attributes were evaluated periodically for 14 days of storage at 4 °C. Although after 1 day of storage TP treatments at level of 1% did not exert any antioxidant effects on TBARS, PV varied for all treatments except control and remained lower than 8 meq O2/kg throughout the storage time. During refrigerated storage, formation of lipid oxidation products increased from 2.8 to 15.2 meq O2/ kg for PV and 0.064 to 0.38 mg malondialdehyde (MDA)/kg in the TBARS test, respectively. At the end of storage time, the PV and MDA value in chicken sausage treated with 1%, 2% and 10% TP decreased by 51 and 19%, 73 and 69%, and 71 and 82% (P <0.05), respectively. The results of sensory evaluation showed that panelists preferred functional sausage containing 2% of TP and higher levels of TP altered the visual appearance of product.

Nutrient release and oxidative stability during in vitro digestion of linseed oil emulsions produced from cow milk, soy drink, and green tea extract

The fortification with ω-3 fatty acids is of great interest, but their vulnerability to oxidation can adversely affect the nutritional quality of food. The objective of this study was to emulsify linseed oil in cow milk or soy drink, with or without adding green tea extract, and compare the nutrient release and lipid oxidation during in vitro gastrointestinal digestion. A protein-free emulsion, prepared with Tween 20, was also studied. The soy-based emulsions showed the highest fatty acid release, but exhibited lower proteolysis in comparison with the cow milk emulsions. Emulsions produced with Tween 20 were the most sensitive to oxidation during digestion, while the emulsions prepared in soy drink were more stable than the emulsions prepared in cow milk. The aggregation pattern of oil droplets under gastric conditions was shown to contribute to the emulsion oxidative stability. Green tea extract reduced the oxidative degradation and acted synergistically with cow milk and soy drink to reduce the formation of lipid oxidation products during digestion. This study shows the potential of cow milk and soy drink constituents, combined to green tea, to enhance the oxidative stability during digestion of emulsions rich in ω-3 fatty acids.

Monitoring Oxidative Degradation of Thermally Stressed Palm Olein Shortening by Spectroscopic and Chromatographic Techniques

Deep frying with repeated use of same edible oil leads to the formation of lipid oxidation products. The presence of these oxidized products formed during frying at elevated temperature is hazardous for human health and therefore, requires prompt analysis for ensuring its fitness/quality. In this study, oxidative degradation of thermally stressed edible oils canola, sunflower and palm olein shortening was studied at 180&#176C ± 5&#176C up to 48 hours. Palm olein shortening remained stable during this period as the increase in its acid value was significantly less than canola and sunflower seed oils. The shortening samples were further studied by attenuated total reflectance Fourier transformation infrared (ATR-FTIR) and gas chromatography mass spectrometry (GC-MS) to evaluate the formation of various oxidation products due to thermal stress. ATR-FTIR indicates the formation of free fatty acids (FFAs), aldehyde groups and change in degree of unsaturation while GC-MS gives important information about profile of FFAs. The combination of these analytical techniques is useful for rapid and highly sensitive analysis of oxidized edible oil thus, ensuring its quality and fitness for safe use.

Effect of Deep-Fat Frying Performance on Canola Oil, Palm Olein and Sunflower Oil Blends: A- Chemical Parameters

Deep-fat frying process produces desirable and undesirable compounds that can cause impairments to the quality of frying of different oils and the fried foods produced. The quality and stability of frying oils are therefore of concern to food technologists, nutritionists, and consumers. The present study was performed to investigate performance of canola oil (CO) and its blends with either sunflower oil (CO+SF) or palm olein (CO+PO) blended at 1:1( w: w) by using different frying cycles of potato chips up to consecutive 10 frying cycle/ 3 day for each oil /days. Significant chemical changes in the frying oil quality have been occurred during frying process. Different chemical deterioration parameters: Iodine value (IV), Free fatty acid (FFA), Peroxide value (PV), Ansidine value (An.v), Totox value, conjugateddienes , total polar compounds (TPC), fatty acids composition (FAs) and Fourier transform infrared (FTIR) of these frying canola oil and blends were investigated .The conjugated dienes at 232nm throughout the frying periods were the lowest (3.12) in CO+PO with the highest(43.04) value in CO+SF after 30 frying cycles. At the end of frying period, CO+SF had the lowest ratio of TPC 2.15 than found in CO+SF F30 and CO F30 (23.88 and 18.2), respectively. Generally, all blends did not exceed the 25% cut-off point for rejecting used frying oil. The blend of CO+PO was the superior in regard to frying stability and lowering TPC after deep-fat frying process.The results of 30 potatoes deep-frying cycles in CO and its blends due to higher saturation, which can be seen from the chemical parameters and (FTIR) data. FTIR provides very useful information about the chemical compositionand impaired in oil quality during thermal oxidation, which is equivalent to that used in the ordinary food preparation.Furthermore FTIR method predicting a modification in the oil’s nutritional value. The results showed that FAs of blends, that contain PO had oxidative stability for the most of fatty acids with lower values than those occurred in frying of CO or CO+SF oils after 30 frying cycles. Furthermore, these results showed evidence that, the oxidation rate for PO in monounsaturated fatty acids (ƩMUSFAs) is much slower than that of the polyunsaturated fatty acids (ƩPUFAs). The ƩMUSFAs, were oxidized, and lower adverse contributed to the improvement of CO stability. Oil blends and frying process caused modifications in the FAs compositions and ω-3/ω-6 ratio.These results indicated that frying may be hazardous due to the formation of lipid oxidation products as a result of thermal degradation of lipids during deep- fat frying process. Therefore in the CO+PO oil blend provided a frying oil alternative for the production deep–fried food, delivering low proportions of trans and saturated fatty acids.

Formation of oxidation products in edible vegetable oils analyzed as FAME derivatives by HPLC-UV-ELSD

Formation of lipid oxidation products was evaluated in dietary vegetable oils by using a novel analytical approach that consisted of derivatization of TAG into FAME and HPLC analysis with two detectors in series, UV and evaporative light scattering detector (ELSD). Three sunflower oils with different contents of oleic and linoleic acids, i.e., high-linoleic (HLSO), high-oleic (HOSO) and high-stearic high-oleic (HSHOSO), and two oils containing linolenic acid, soybean (SbO) and rapeseed (RO) oils, were heated at 40°C and analyzed up to the total exhaustion of tocopherols. Results showed that oxidation products of linoleate were predominant in all cases, whereas no significant formation of oleate oxidation products was observed in the five oils in the presence of substantial contents of the tocopherols naturally occurring. Formation of oleate hydroperoxides and monoepoxystearates derived from oleic acid was only detected when tocopherols were exhausted in the monounsaturated oils, i.e., HOSO, HSHOSO and RO. The analysis of the main oxidation products of linoleate by the method applied proved to be a good analytical approach to evaluate the global oxidation extent of oils containing oleic and linoleic acids as the only oxidizable substrates. The method used enabled the quantitative determination of the simple hydroperoxydienes of linoleate and linolenate as a whole. Results suggested occurrence of hydroperoxy compounds other than those determined by the method in the oils containing linolenic acid, showing the low stability of simple hydroperoxydienes and their participation in further reactions.

Lipid Quality of Anchovy (Engraulis Encrasicholus) Fillets Affected by Different Cooking Methods

The influence of cooking methods (baking, grilling, or frying) on lipid oxidation and fatty acid composition of anchovy (Engraulis encrasicholus) fillets was evaluated. All of the treatments reduced the free fatty acid content of the fillets (P < 0.05) and minimal values were determined in grilled (3.30 g/100 g lipid) and fried (2.84 g/100 g lipid) fillets. The peroxide value and thiobarbituric acid value of the fillets were also increased by the cooking process (P < 0.05). While the maximum peroxide value content of anchovy fillets was determined in grilled fillets as 16.23 meq O2/kg lipid (P < 0.05), the highest thiobarbituric acid values were determined as 3.63 mg MDA/kg fillet and 2.96 mg MDA/kg fillet for grilled and baked fillets, respectively. In the grilled fillets, the increase of thiobarbituric acid value exceeded the permitted limiting value. All of the cooking methods used caused modifications in the fatty acid compositions and only frying caused modification in the n-3/n-6 ratio of the fillets. The modifications in the fatty acid compositions were more prominent in the fried fillets. These results indicated that grilling may be hazardous because of the formation of lipid oxidation products as a result of thermal degradation of lipids during cooking.

Galloylated Polyphenols as Inhibitors of Hemoglobin-Catalyzed Lipid Oxidation in Fish Muscle

The influence of galloyl residues on the antioxidant mechanism of polyphenols to prevent hemoglobin-promoted lipid oxidation was investigated by using polyphenolic fractions with different degrees of galloylation: nongalloylated structures from pine bark (IVP), medium-galloylated from grape pomace (IVG), and high-galloylated from witch hazel bark (IVH). Hemoglobin (Hb) from the pelagic fish horse mackerel (Trachurus trachurus) was employed as a Hb standard. In vitro experiments showed an important increase in the deoxygenation and autoxidation of horse mackerel Hb at acidic pH values. All polyphenolic fractions significantly reduced the redox stability of Hb in buffer solutions, showing a greater deoxygenation and methemoglobin (metHb) formation in the presence of IVH, followed in decreasing order by IVG and IVP. However, galloylated polyphenols (IVH and IVG) were efficient to inhibit the oxidation of the oxygenated Hb (OxyHb) and the formation of lipid oxidation products in chilled washed fish muscle. This antioxidant activity of galloylated proanthocyanidins showed a positive relationship with the phenolic concentration. Polyphenols devoid of galloyl groups (IVP) were less active to prevent either Hb oxidation or lipid oxidation in fish muscle. The results draw attention to the potential role of galloyl residues to lessen Hb-catalyzed lipid oxidation in muscle and to maintain Hb in reduced and oxygenated states, which exhibit lower pro-oxidant activity as compared to the metHb and deoxyHb species.

Development of functional bread containing nanoencapsulated omega-3 fatty acids

The aim of this study was to develop functional bread enriched with omega-3 fatty acids. High amylose corn starch was used to form nanosized complexes with flax seed oil that was converted to powder of microparticles by spray drying. The particles were then incorporated into bread formulation at different amounts to investigate their effects on bread quality characteristics. The effects of encapsulation on the formation of lipid oxidation products and thermal process contaminants including acrylamide and hydroxymethyl furfural (HMF) were determined. Encapsulation significantly decreased lipid oxidation as measured by the formation of hexanal and nonanal in breads during baking. Increasing the amount of particles in dough significantly decreased the formation of acrylamide and HMF in breads. Scanning electron microscopic analysis of bread demonstrated that particles added to dough remained intact in the crumb, but partially destroyed in the crust. Comparing to its free form, addition of nanoencapsulated flax seed oil increased final product quality and safety by lowering lipid oxidation and formation of harmful compounds in breads during baking.