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

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.

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Ella Baker ◽  
Elizabeth Miles ◽  
Philip Calder

AbstractHigh consumption of ω-3 long chain polyunsaturated fatty acids (PUFAs) has long-term health benefits. The principal dietary source of these ω-3 PUFAs (eicosapentaenoic acid, EPA and docosapentaenoic acid, DHA) is seafood, particularly oily fish. However current fish stocks are decreasing, indicating a need for alternative sources of bioactive PUFAs. Plant-derived ω-3 PUFAs (alpha-linolenic acid, ALA and stearidonic acid, SDA) may be able to provide land-based sustainable sources, but their functionality has been underexplored.Anti-inflammatory effects of ALA and SDA were compared to EPA and DHA in cultured EA.hy926 endothelial cells. Cells were treated with PUFAs (10, 25 and 50 μM) for 48 hours prior to stimulation with tumour necrosis factor for 24 hours. PUFAs incorporation was measured by gas chromatography and inflammatory responses were measured by ELISA, RT-PCR, western blot and flow cytometry. Adhesion of THP-1 monocytes to EA.hy926 cells was determined using a static adhesion assay.All PUFAs were incorporated into EA.hy926 cells in a dose-dependant manner (10 and 50 μM). Pre-treatment with ALA, SDA, EPA and DHA (50 μM) had differential effects on inflammatory responses in EA.hy926 cells depending on PUFA and response examined.EA.hy926 cells pre-treated with SDA had lower concentrations of soluble ICAM-1 (p < 0.05); however EPA and DHA resulted in greater reduction (p < 0.0001). EPA and DHA pre-treated EA.hy926 cells had significantly lower concentrations of IL-6 (p < 0.0001), IL-8 (p < 0.0001) and MCP-1 (p < 0.05, p < 0.01). ALA pre-treatment did not significantly affect any of the cytokines examined. Lower cell surface expression of ICAM-1 (p < 0.05), was seen for EA.hy926 cells pre-treated with SDA again to a lesser extent than EPA and DHA (p < 0.001, p < 0.0001), with no effect seen after ALA treatment.EA.hy926 cells pre-treated with ALA had significantly higher relative gene expression of NFKB (p < 0.05), as well as a tendency for more phosphorylated NFKBp65 protein (p < 0.06). In contrast, EA.hy926 cells pre-treated with DHA had significantly less phosphorylated NFKB (p < 0.0001). EA.hy926 cells with DHA treatment had significantly higher relative gene expression of PPARa (p < 0.05). SDA and EPA had no effect on expression of either of the genes or proteins examined.Finally pre-treatment with ALA, SDA and DHA all resulted in reduced adhesion of THP-1 monocytes to EA.hy926, however this effect not observed with EPA.Marine derived PUFA, particularly DHA, resulted in potent anti-inflammatory effects within this endothelial cell model. Of the two plant derived PUFAs, SDA treatment lead to some anti-inflammatory effects, which were not seen after treatment with ALA.


Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3078
Author(s):  
Irina A. Guschina ◽  
Natalia Ninkina ◽  
Andrei Roman ◽  
Mikhail V. Pokrovskiy ◽  
Vladimir L. Buchman

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.


2021 ◽  
Vol 11 (15) ◽  
pp. 7144
Author(s):  
Muriel C. Bischof ◽  
Sonja Häckel ◽  
Andrea Oberli ◽  
Andreas S. Croft ◽  
Katharina A. C. Oswald ◽  
...  

Increasing evidence implicates intervertebral disc (IVD) degeneration as a major contributor to low back pain. In addition to a series of pathogenic processes, degenerated IVDs become vascularized in contrast to healthy IVDs. In this context, angiopoietin (Ang) plays a crucial role and is involved in cytokine recruitment, and anabolic and catabolic reactions within the extracellular matrix (ECM). Over the last decade, a progenitor cell population has been described in the nucleus pulposus (NP) of the IVD to be positive for the Tie2 marker (also known as Ang-1 receptor). In this study, we investigated the influence of Ang-1 and Ang-2 on human NP cell (Tie2+, Tie2- or mixed) populations isolated from trauma patients during 7 days in normoxia (21% O2) or hypoxia (≤ 5% O2). At the end of the process, the proliferation and metabolic activity of the NP cells were analyzed. Additionally, the relative gene expression of NP-related markers was evaluated. NP cells showed a higher proliferation depending on the Ang treatment. Moreover, the study revealed higher NP cell metabolism when cultured in hypoxia. Additionally, the relative gene expression followed, with an increase linked to the oxygen level and Ang concentration. Our study comparing different NP cell populations may be the start of new approaches for the treatment of IVD degeneration.


Author(s):  
D.L. Silva ◽  
B.R. Carvalho ◽  
H.C. Ferreira Júnior ◽  
H.C. Oliveira ◽  
C.R. Ferreira ◽  
...  

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