Permeability and membrane lipid metabolism of Phaseolus vulgaris infected with Uromyces phaseoli IV. Phospholipids and phospholipid fatty acids in healthy and rust-infected bean leaves resistant and susceptible to Uromyces phaseoli

1975 ◽  
Vol 5 (3) ◽  
pp. 263-271 ◽  
Author(s):  
H.H. Hoppe ◽  
R. Heitefuss
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.


2020 ◽  
Author(s):  
Irina Guschina ◽  
Natalia Ninkina ◽  
Andrei Y. Roman ◽  
Mikhail V. Pokrovskiy ◽  
Vladimir L. Buchman

Abstract Background: 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. All members of the synuclein family interact robustly with lipid membranes, and appear to be important for the physiological functions of proteins while influencing the pathological aggregation of α-synuclein. Methods: The following tissues were used for lipid and fatty acid analysis: plasma, liver and two brain areas (cortex and midbrain). Lipid classes were separated using thin-layer chromatography. Fatty acids were analysed using gas chromatography. Results: We describe the importance of long-chain polyunsaturated fatty acids (LCPUFA) and palmitic acid in liver and plasma, reduced triacylglycerol (TAG) accumulation in liver and circulated plasma non-esterified fatty acids in synuclein free mice. In midbrain, observed changes in the relative concentrations of phosphatidylcholine (PC) and cerebrosides (CER) were counterbalanced. In midbrain, we recorded a notable reduction in ethanolamine plasmalogens in synuclein free mice and consider this an important finding considering the abnormal ether lipid metabolism usually associated with neurological disorders.Conclusions: In summary, our data demonstrate that synuclein deficiency can result in alterations of PUFA synthesis, storage lipid accumulation in liver, and 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 resulted in more pronounced lipid modifications then previously showed by us γ-synuclein deficiency. Possible mechanisms by which synuclein deficiency may govern the reported modifications of lipid metabolism in TKO mice are proposed and discussed.


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 27 ◽  
Author(s):  
Justyna Dłubek ◽  
Jacek Rysz ◽  
Zbigniew Jabłonowski ◽  
Anna Gluba-Brzózka ◽  
Beata Franczyk

: Prostate cancer is second most common cancer affecting male population all over the world. The existence of a correlation between lipid metabolism disorders and cancer of the prostate gland has been widely known for a long time. According to hypotheses, cholesterol may contribute to prostate cancer progression as a result of its participation as a signalling molecule in prostate growth and differentiation via numerous biologic mechanisms including Akt signalling and de novo steroidogenesis. The results of some studies suggest that increased cholesterol levels may be associated with higher risk of more aggressive course of disease. The aforementioned alterations in the synthesis of fatty acids are a unique feature of cancer and, therefore, it constitutes an attractive target for therapeutic intervention in the treatment of prostate cancer. Pharmacological or gene therapy aimed to reduce the activity of enzymes involved in de novo synthesis of fatty acids, FASN, ACLY (ATP citrate lyase) or SCD-1 (stearoyl-CoA desaturase) in particular, may result in cells growth arrest. Nevertheless, not all cancers are unequivocally associated with hypocholesterolaemia. It cannot be ruled out that the relationship between prostate cancer and lipid disorders is not a direct quantitative correlation between carcinogenesis and the amount of the circulating cholesterol. Perhaps the correspondence is more sophisticated and connected to the distribution of cholesterol fractions, or even sub-fractions of e.g. HDL cholesterol.


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