Insights into the metabolism of membrane lipid fatty acids associated with chilling injury in post-harvest bell peppers

2019 ◽  
Vol 295 ◽  
pp. 26-35 ◽  
Author(s):  
Wanying Ge ◽  
Ximan Kong ◽  
Yingbo Zhao ◽  
Baodong Wei ◽  
Qian Zhou ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Post Harvest ◽  
Bell Peppers

scholarly journals Revealing Further Insights on Chilling Injury of Postharvest Bananas by Untargeted Lipidomics

Foods ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 894 ◽  
Author(s):  
Juan Liu ◽  
Qingxin Li ◽  
Junjia Chen ◽  
Yueming Jiang
Keyword(s):  
Fatty Acids ◽  
Low Temperature ◽  
Unsaturated Fatty Acids ◽  
Membrane Lipids ◽  
Saturated Fatty Acids ◽  
Chilling Injury ◽  
Membrane Damage ◽  
Membrane Lipid ◽  
Banana Fruit ◽  
Control Fruit

Chilling injury is especially prominent in postharvest bananas stored at low temperature below 13 °C. To elucidate better the relationship between cell membrane lipids and chilling injury, an untargeted lipidomics approach using ultra-performance liquid chromatography–mass spectrometry was conducted. Banana fruit were stored at 6 °C for 0 (control) and 4 days and then sampled for lipid analysis. After 4 days of storage, banana peel exhibited a marked chilling injury symptom. Furthermore, 45 lipid compounds, including glycerophospholipids, saccharolipids, and glycerolipids, were identified with significant changes in peel tissues of bananas stored for 4 days compared with the control fruit. In addition, higher ratio of digalactosyldiacylglycerol (DGDG) to monogalactosyldiacylglycerol (MGDG) and higher levels of phosphatidic acid (PA) and saturated fatty acids but lower levels of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and unsaturated fatty acids were observed in banana fruit with chilling injury in contrast to the control fruit. Meanwhile, higher activities of phospholipase D (PLD) and lipoxygenase (LOX) were associated with significantly upregulated gene expressions of MaPLD1 and MaLOX2 and higher malondialdehyde (MDA) content in chilling injury-related bananas. In conclusion, our study indicated that membrane lipid degradation resulted from reduced PC and PE, but accumulated PA, while membrane lipid peroxidation resulted from the elevated saturation of fatty acids, resulting in membrane damage which subsequently accelerated the chilling injury occurrence of banana fruit during storage at low temperature.

scholarly journals Cold shock treatment alleviates chilling injury in peach fruit by regulating antioxidant capacity and membrane lipid metabolism

2022 ◽  
Vol 6 ◽  
Author(s):  
Yuqing Ma ◽  
Shunqing Hu ◽  
Guifang Chen ◽  
Yonghua Zheng ◽  
Peng Jin
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Cold Shock ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Membrane Fatty Acid ◽  
Relative Gene Expression ◽  
Peach Fruit ◽  
Relative Gene

Abstract Objectives The work intended to reveal the effect of cold shock (CS) treatment on chilling injury (CI), antioxidant capacity, and membrane fatty acid of peach fruit. Materials and methods Peaches were soaked in ice water (0 °C) for 10 min and stored at 5 °C for 28 days for determination, except CI, and then stored for 3 days at 20 °C, only CI was measured. The electrolyte leakage (EL) was measured by conductivity meter. The activities of antioxidant enzymes (superoxide dismutase, ascorbate peroxidase, catalase, and peroxidase) and key enzymes of membrane lipid metabolism (phospholipase D, lipase, and lipoxygenase) as well as reactive oxygen species (ROS; O2·– and H2O2) were measured with a spectrophotometer. An ELISA kit and gas chromatography were used to determine membrane lipids and membrane fatty acids. The relative gene expression was measured by real-time polymerase chain reaction analysis. Results The results showed that CS treatment effectively delayed CI, suppressed the increase of EL and malondialdehyde content. Meanwhile, CS-treated fruit exhibited lower level of ROS and higher activities of antioxidant enzymes. Furthermore, CS treatment inhibited the activities as well as the relative gene expression of key enzymes in membrane lipid metabolism. CS-treated fruits maintained higher membrane fatty acid unsaturation and lower phosphatidic acid content. Conclusions These results indicated that CS treatment effectively alleviated CI and maintained the integrity of cell membranes by inducing antioxidant-related enzyme activity and maintaining a higher ratio of unsaturated fatty acids to saturated fatty acids.

Transcription factor CaNAC1 regulates low-temperature-induced phospholipid degradation in green bell pepper

2019 ◽  
Author(s):  
Xi-man Kong ◽  
Qian Zhou ◽  
Xin Zhou ◽  
Bao-dong Wei ◽  
Shu-juan Ji
Keyword(s):  
Transcription Factor ◽  
Low Temperature ◽  
Low Temperatures ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Mobility Shift ◽  
Low Temperature Storage ◽  
Bell Peppers ◽  
Main Component ◽  
Phospholipid Degradation

Abstract Phospholipids constitute the main component of biomembranes. During low-temperature storage and transportation of harvested bell peppers, chilling injury participates in pepper decay. A primary cause of pepper chilling injury is phospholipid degradation. In this study, three phospholipase D (PLD)-encoding genes were identified from bell peppers and their activity were analyzed under cold stress. Low temperatures induced strong accumulation of the CaPLDα4 transcript, suggesting that this induction contributes to the phenomenon of phospholipid degradation and cell membrane destruction at 4°C. Low temperatures also significantly induced the transcript amounts of NAM-ATAF1/2-CUC2 (NAC) domain transcription factor. CaNAC1 was found to possess the capacity to interact with the promoter of CaPLD4 in a yeast one-hybrid screen. Furthermore, electrophoretic mobility shift and ß-glucuronidase reporter assays demonstrated that CaNAC1 binds to the CTGCAG motif in the CaPLDα4 promoter, thereby activating its transcription and controlling phospholipid degradation. The ubiquitination sites of the CaNAC1 protein were also characterized by liquid chromatography tandem-mass spectrometry. In conclusion, CaNAC1 is a transcriptional activator of CaPLDα4 and is suggested to participate in membrane lipid degradation of bell peppers when stored at low temperature.

scholarly journals Changes in Membrane Lipid Composition and Function Accompanying Chilling Injury in Bell Peppers

2017 ◽  
Vol 59 (1) ◽  
pp. 167-178 ◽  
Author(s):  
Ximan Kong ◽  
Baodong Wei ◽  
Zhu Gao ◽  
Ying Zhou ◽  
Fei Shi ◽  
...  
Keyword(s):  
Lipid Composition ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Membrane Lipid Composition ◽  
Bell Peppers ◽  
And Function

scholarly journals Triple-Knockout, Synuclein-Free Mice Display Compromised Lipid Pattern

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3078
Author(s):  
Irina A. Guschina ◽  
Natalia Ninkina ◽  
Andrei Roman ◽  
Mikhail V. Pokrovskiy ◽  
Vladimir L. Buchman
Keyword(s):  
Fatty Acids ◽  
Lipid Metabolism ◽  
Family Members ◽  
Ether Lipid ◽  
Brain Regions ◽  
Membrane Lipid ◽  
Lipid Binding ◽  
Synaptic Functions ◽  
Ethanolamine Plasmalogens ◽  
Lipid Pattern

Recent studies have implicated synucleins in several reactions during the biosynthesis of lipids and fatty acids in addition to their recognised role in membrane lipid binding and synaptic functions. These are among aspects of decreased synuclein functions that are still poorly acknowledged especially in regard to pathogenesis in Parkinson’s disease. Here, we aimed to add to existing knowledge of synuclein deficiency (i.e., the lack of all three family members), with respect to changes in fatty acids and lipids in plasma, liver, and two brain regions in triple synuclein-knockout (TKO) mice. We describe changes of long-chain polyunsaturated fatty acids (LCPUFA) and palmitic acid in liver and plasma, reduced triacylglycerol (TAG) accumulation in liver and non-esterified fatty acids in plasma of synuclein free mice. In midbrain, we observed counterbalanced changes in the relative concentrations of phosphatidylcholine (PC) and cerebrosides (CER). We also recorded a notable reduction in ethanolamine plasmalogens in the midbrain of synuclein free mice, which is an important finding since the abnormal ether lipid metabolism usually associated with neurological disorders. In summary, our data demonstrates that synuclein deficiency results in alterations of the PUFA synthesis, storage lipid accumulation in the liver, and the reduction of plasmalogens and CER, those polar lipids which are principal compounds of lipid rafts in many tissues. An ablation of all three synuclein family members causes more profound changes in lipid metabolism than changes previously shown to be associated with γ-synuclein deficiency alone. Possible mechanisms by which synuclein deficiency may govern the reported modifications of lipid metabolism in TKO mice are proposed and discussed.

Fatty acyl chain structure, orientational order, and the lipid phase transition in Acholeplasma laidlawii B membranes. A review of recent 19F nuclear magnetic resonance studies

1984 ◽  
Vol 62 (11) ◽  
pp. 1134-1150 ◽  
Author(s):  
P. M. Macdonald ◽  
B. D. Sykes ◽  
R. N. McElhaney
Keyword(s):  
Phase Transition ◽  
Fatty Acids ◽  
Nuclear Magnetic Resonance ◽  
Acyl Chain ◽  
Orientational Order ◽  
Membrane Lipid ◽  
Fatty Acyl ◽  
Fatty Acyl Chain ◽  
Lipid Phase ◽  
Lipid Phase Transition

The orientational order parameters of monofluoropalmitic acids biosynthetically incorporated into membranes of Acholeplasma laidlawii B in the presence of a large excess of a variety of structurally diverse fatty acids have been determined via 19F nuclear magnetic resonance (19F NMR) spectroscopy. It is demonstrated that these monofluoropalmitic acids are relatively nonperturbing membrane probes based upon physical (differential scanning calorimetry), biochemical (membrane lipid analysis), and biological (growth studies) criteria. 19F NMR is shown to convey the same qualitative and quantitative picture of membrane lipid order provided by 2H-NMR techniques and to be sensitive to the structural characteristics of the membrane fatty acyl chains, as well as to the lipid phase transition. Representatives of each naturally occurring class of fatty acyl chain structures, including straight-chain saturated, methyl-branched, monounsaturated, and alicyclic-ring-substituted fatty acids, were studied and the 19F-NMR order parameters were correlated with the lipid phase transitions (determined calorimetrically). The lipid phase transition was the prime determinant of overall orientational order regardless of fatty acid structure. Effects upon orientational order attributable to specific structural substituents were discernible, but were secondary to the effects of the lipid phase transition. In the gel state, relative overall order was directly proportional to the temperature of the particular lipid phase transition. Not only the overall order, but also the order profile across the membrane was sensitive to the presence of particular structural substituents. In particular, in the gel state specific fatty acyl structures demonstrated a characteristic disordering effect in the membrane order profile. These various observations can be merged to provide a unified picture of the manner in which fatty acyl chain chemistry modulates the physical state of membrane lipids.

scholarly journals Palmitic acid promotes resistin-induced insulin resistance and inflammation in SH-SY5Y human neuroblastoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hamza Amine ◽  
Yacir Benomar ◽  
Mohammed Taouis
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Palmitic Acid ◽  
Lipid Rafts ◽  
Acid Treatment ◽  
Protective Action ◽  
Saturated Fatty Acids ◽  
Membrane Lipid ◽  
Human Neuroblastoma ◽  
Peripheral Tissues

AbstractSaturated fatty acids such as palmitic acid promote inflammation and insulin resistance in peripheral tissues, contrasting with the protective action of polyunsaturated fatty acids such docosahexaenoic acid. Palmitic acid effects have been in part attributed to its potential action through Toll-like receptor 4. Beside, resistin, an adipokine, also promotes inflammation and insulin resistance via TLR4. In the brain, palmitic acid and resistin trigger neuroinflammation and insulin resistance, but their link at the neuronal level is unknown. Using human SH-SY5Yneuroblastoma cell line we show that palmitic acid treatment impaired insulin-dependent Akt and Erk phosphorylation whereas DHA preserved insulin action. Palmitic acid up-regulated TLR4 as well as pro-inflammatory cytokines IL6 and TNFα contrasting with DHA effect. Similarly to palmitic acid, resistin treatment induced the up-regulation of IL6 and TNFα as well as NFκB activation. Importantly, palmitic acid potentiated the resistin-dependent NFkB activation whereas DHA abolished it. The recruitment of TLR4 to membrane lipid rafts was increased by palmitic acid treatment; this is concomitant with the augmentation of resistin-induced TLR4/MYD88/TIRAP complex formation mandatory for TLR4 signaling. In conclusion, palmitic acid increased TLR4 expression promoting resistin signaling through TLR4 up-regulation and its recruitment to membrane lipid rafts.

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