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To investigate the effect of n-butanol on postharvest membrane lipid metabolism of Hami melon (Cucumis melo ‘Hami’), the fruits were soaked in a 1.0% solution of n-butanol for 30 min with water as the control. Symptoms of chilling injury were observed regularly, and the indices related to permeability and membrane lipid metabolism of pericarp cells were measured. The results showed that treatment with n-butanol inhibited the increase in chilling injury index, membrane permeability, and malondialdehyde content of Hami melon fruits, promoted an increase in the contents of phosphatidyl alcohol and unsaturated fatty acids, such as linoleic acid, linolenic acid, oleic acid (except 14 d), and erucic acid (28–42 d), and decreased the content of saturated fatty acids, stearic acid (0–28 d), phosphatidic acid (except for 21 d), and the key enzymes of membrane lipid metabolism compared with the control. The activities of phospholipase D (PLD) and lipoxygenase (LOX) and the downregulation of the levels of expression CmPLD-β and CmLOX (42 d only) genes reduced the chilling injury index of Hami melon and alleviated the further expansion of chilling injury symptoms in the fruits. We also cloned the key gene of membrane lipid metabolism CmPLD-β, which was obtained by pre-transcriptome screening of the pericarp. We found that CmPLD-β of Hami melon had the closest affinity with cucumber (CsXP5), indicating that the CmPLD-β gene of Hami melon was functionally similar to that of cucumber. In addition, a two-fold alignment analysis of CmPLD-β and CmXP5 base sequences indicated that the base sequences of the two promoter regions differed from each other.

Cucumber fruit is very sensitive to chilling injury, which rapidly depreciates their commodity value. Herein, the effect of fucoidan treatment on cucumber under cold stress were investigated. Fucoidan treatment of cold-stored cucumber alleviated the occurrence of chilling injury, delayed weight loss, lowered electrolyte leakage and respiration rate, and retarded malondialdehyde accumulation. Different from the control fruit, fucoidan treated fruit showed a high level of fatty acid unsaturated content, fatty acid unsaturation, and unsaturation index and increased ω-FDAS activity, along with upregulated expression levels of CsSAD and CsFAD genes. Fucoidan reduced the phosphatidic acid content and membrane lipid peroxidation, lowered the phospholipase D (PLD) and lipoxygenase (LOX) activity, and downregulated the expression levels of CsPLD and CsLOX genes. Collectively, fucoidan treatment maintained the integrity of cell membrane in cold-stress cucumbers. The results provide a new prospect for the development of fucoidan as a preservative agent in the low-temperature postharvest storage of cucumbers.

Banana fruit is a widely cultivated and economically important crop, and it is susceptible to mechanical damage. The effects of three different phospholipase D inhibitors (0.1% n-butanol, 0.05% 2-butanol, and 0.1% hexanal) on the cell membrane integrity and membrane lipid metabolism in wounding banana fruits during storage were investigated. The results indicated that wounded banana treated with phospholipase D inhibitors showed significant (p < 0.05) delay in the ripening and senescence process than the control group after a 9-day storage. Of the three PLD inhibitors, hexanal showed the best effect in maintaining firmness, suppressing the increase of total soluble solids (TSS) and respiration rate, and reducing malondialdehyde (MDA) content and cell membrane permeability of wounded banana fruits. Furthermore, hexanal more efficiently decreased the phospholipase D (PLD) and lipoxygenase (LOX) activities, lowered the contents of phosphatidic acid (PA) and diacylglycerol (DAG), and inhibited the reduction of phosphatidylcholine (PC) and phosphatidylinositol (PI) after 6 days of storage, compared to n-butanol or 2-butanol. These results demonstrate that application of hexanal treatment may be a reliable method to delay the senescence of harvested bananas subjected to mechanical wounding.

1‐MCP is an ethylene inhibitor which can delay the ripening and senescence of fruits and vegetables effectively. Pteridium aquilinum var. Latiusculum (PA) is one of the wild vegetables which is famous and nutrient in China. However, the mechanism of PA preservation treated with 1‐MCP has not been reported. Consequently, the effects of postharvest 1‐MCP treatment on the changes in quality, energy metabolism, and membrane lipid metabolism of PA were investigated in this study. The results indicated that 1‐MCP treatment could effectively inhibit the decreases in firmness, titratable acid (TA) content and the increases in weight loss rate, malondialdehyde (MDA) content, membrane permeability, and membrane lipid metabolism‐related enzymes in PA. The cellular energy charge (EC) and the levels of ATP, ATP/ADP, and ATP/AMP, the activities of energy metabolism‐related enzymes, NAD+, and NADH were maintained, and the decreases in unsaturated fatty acids and the ratio of unsaturated‐to‐saturated fatty acids in the membrane of PA cells were effectively retarded by 1‐MCP treatment. A positive correlation was observed between cellular ATP levels and the ratio of unsaturated‐to‐saturated fatty acids, while negative correlations were observed between the ratio of unsaturated‐to‐saturated fatty acids and both lipid peroxidation and membrane permeability. These results indicated that higher levels of energy status, unsaturated‐to‐saturated fatty acid ratios, and lipid metabolism in the membrane could preserve the membrane integrity of postharvest PA and effectively extend its shelf life., 1‐MCP treatment could affect the quality, energy status, membrane lipid metabolism, membrane fatty acids, the activities of energy‐metabolism‐related enzymes, and lipid metabolism‐related enzymes of postharvest Pteridium aquilinum var. latiusculum (PA). The results indicated that 1‐MCP treatment could extend the shelf life of PA effectively.

Sweet sorghum has strong stress resistance and is considered a promising energy crop. In the present study, the effects of salt on the membrane lipid metabolism of two sweet sorghum inbred lines (salt-tolerant M-81E and salt-sensitive Roma) were analyzed. After treatment with 150 mM NaCl, higher levels of fresh weight and chlorophyll fluorescence, as well as lower levels of malondialdehyde (MDA) were found in salt-tolerant M-81E. Concomitantly, 702 and 1339 differentially expression genes (DEGs) in M-81E and Roma were identified in response to salt stress. We determined that most DEGs were related to glycerophospholipid metabolism, glycerolipid metabolism, and other membrane lipid metabolisms. Under NaCl treatment, the expression of the membrane-associated phospholipase A1 was down-regulated at the transcriptional level, along with an increased content of phosphatidylcholine (PC) in both cultivars. The inhibition of triacylglycerol (TAG) mobilization in M-81E delayed salt-induced leaf senescence. Furthermore, enhanced levels of glycerol-3-phosphate acyltransferase (GPAT) expression contributed to improved salt resistance in M-81E. The results of this study demonstrate membrane the role of lipid regulation in mediating salt-defensive responses in sweet sorghum and expand our understanding of the relationship between changes in membrane lipid content and salt resistance.

Mild stress could help cells to survive more severe environmental or pathophysiological conditions. In the current study, we investigated the cellular mechanisms which contribute to the development of stress tolerance upon a prolonged (0–12 h) fever-like (40 °C) or a moderate (42.5 °C) hyperthermia in mammalian Chinese Hamster Ovary (CHO) cells. Our results indicate that mild heat triggers a distinct, dose-dependent remodeling of the cellular lipidome followed by the expression of heat shock proteins only at higher heat dosages. A significant elevation in the relative concentration of saturated membrane lipid species and specific lysophosphatidylinositol and sphingolipid species suggests prompt membrane microdomain reorganization and an overall membrane rigidification in response to the fluidizing heat in a time-dependent manner. RNAseq experiments reveal that mild heat initiates endoplasmic reticulum stress-related signaling cascades resulting in lipid rearrangement and ultimately in an elevated resistance against membrane fluidization by benzyl alcohol. To protect cells against lethal, protein-denaturing high temperatures, the classical heat shock protein response was required. The different layers of stress response elicited by different heat dosages highlight the capability of cells to utilize multiple tools to gain resistance against or to survive lethal stress conditions.

Browning has been the primary limitation in eggplant processing. This study investigates the molecular mechanism underlying fresh-cut eggplant fruit browning by observing the physicochemical characteristics of browning-resistant (‘F’) and browning-sensitive (‘36′) eggplant cultivars. Browning-related enzyme activity and gene expression (PPO, LOX, and PLD) were significantly higher in the ‘36′ eggplant, thereby enhancing the degree of browning, compared to the ‘F’ eggplant. The MDA content and O2− production rate progressively increased as browning increased, while the antioxidant capacity of the fruit decreased. The cutting injury significantly activated the expression of PAL, thereby inducing the accumulation of phenolic acids, while the PPO gene was significantly upregulated, which activated the activity of polyphenol oxidase. Our results showed that the oxidation of chlorogenic acids to chlorogenic quinones resulted in the occurrence of browning, which suggests chlorogenic acid as the main browning substrate in fresh-cut eggplant.

Horticultural commodities suffer chilling injury following exposure to extremely low temperatures, which results in visible symptoms and considerable quality loss. Therefore, it is of significance to understand the mechanism of this physiological disorder and to develop effective strategies to control it. Chilling stress causes alteration in structure and function of the plasma membrane, which is assumed to be the primary event in response to cold stress. During this process, the membrane lipid metabolism plays a pivotal role in membrane fluidity and stability. In this review, we summarized the possible roles of membrane lipid metabolism in the development of chilling injury, having the potential for developing effective strategies to alleviate chilling injury in horticultural products under refrigerated storage in practice.

Early sowing has been extensively used in high-latitude areas to avoid drought stress during sowing; however, cold damage has become the key limiting factor of early sowing. To relieve cold stress, plants develop a series of physiological and biochemical changes and sophisticated molecular regulatory mechanisms. The biomembrane is the barrier that protects cells from injury as well as the primary place for sensing cold signals. Chilling tolerance is closely related to the composition, structure, and metabolic process of membrane lipids. This review focuses on membrane lipid metabolism and its molecular mechanism, as well as lipid signal transduction in peanut (Arachis hypogaea L.) under cold stress to build a foundation for explicating lipid metabolism regulation patterns and physiological and molecular response mechanisms during cold stress and to promote the genetic improvement of peanut cold tolerance.

Since the organism contains many redundant reactions, the minimal feasible metabolic network that contains the basic growth function is not the collection of reactions that associate the essential genes. To identify minimal metabolic reaction set is a challenging work in theoretical approach. A new method is presented here to identify the smallest required reaction set of growth-sustaining metabolic networks. The content and number of the minimal reactions for growth are variable in different random processes. Though the different carbon sources also vary the content of the reactions in the minimal metabolic networks, most essential reactions locate in the same metabolic subsystems, such as cofactor and prosthetic group biosynthesis, cell envelope biosynthesis, and membrane lipid metabolism.

Phosphoinositides, the phosphorylated products of inositol phospholipids, play critical regulatory roles in cell physiology. The elucidation of their functions will greatly benefit from the methodology to manipulate their local concentrations within membranes with high spatial and temporal precision. Recently developed genetically encoded and light-regulated dimerization modules, in combination with the use of fluorescence-tagged lipid-binding domains and live-cell imaging, provide an attractive means to achieve this goal. Here we describe a protocol for blue light-dependent conversion of one phosphoinositide species into another based on the light-regulated dimerization between cryptochrome 2 (CRY2) and its ligand, CIB1. We describe the development of these tools using the dephosphorylation of plasma membrane phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) as an example and show how they can be used to rapidly and reversibly deplete the plasma membrane of this lipid. We also provide instructions for image analysis. The CRY2-CIB1 dimerization method has also already been adapted for the acute and spatially restricted generation of PI(3,4,5)P3 in the plasma membrane. More generally, this methodology should be broadly applicable to studies of the spatiotemporal regulation of membrane lipid metabolism in many types of cells.

Batten disease (juvenile neuronal ceroid lipofuscinosis) is a severe, untreatable, inherited neurodegenerative disease. Biochemical studies have revealed a marked deficiency of phospholipids in red...

Phospholipids and phospholipid fatty acids were determined in healthy and rust-infected primary leaves of six bean varieties, resistant and susceptible to Uromyces phaseoli. In bean leaves of susceptible and resistant varieties PCH was the major phospholipid followed by PG, PE and PI, whereas PA, PS, DPG and PX appeared only in low concentrations. The main fatty acids detected in PCH, PG and PE were palmitic, stearic, oleic, linoleic, linolenic and in PG trans-3-hexadecenoic acid. In the susceptible varieties the infection resulted in an increase in PS and a decrease in PG content. The PE and PCH isolated from infected leaves of susceptible varieties contained a higher amount of unsaturated fatty acids than the lipids from control leaves. In the hypersensitive reacting varieties the infection resulted in a decrease in PG content. The changes observed in phospholipid and phospholipid fatty acids in bean leaves after infection were not related to resistance or susceptibility.

The leakage of electrolytes, amino acids and sugars from rust-infected leaf halves and uninfected halves of the same leaves was determined and compared with the leakage from healthy primary leaves of bean plants. The infection brought about a significant increase in the leakage of ions, amino acids and sugars from the infected leaf halves. The leakage became evident at 4 days after inoculation and was further increased for electrolytes and amino acids during the remainder of the experimental period. No differences were observed between the uninfected leaf halves and the controls up to 8 days after inoculation, but afterwards (10 and 12 days after inoculation) the leakage from the uninfected leaf halves was higher.

In this critical review of human in vivo nuclear magnetic resonance (NMR) spectroscopy, the questions of which chemical species can be detected and with what sensitivity, their biochemical significance, and their potential clinical value are addressed. The current in vivo detectability limit is about 10(-6) of that of tissue water protons, necessitating a 1-10 cm3-volume of tissue and approximately 10-minute averaging time. This permits access to fats, membrane lipid metabolism, high-energy phosphate metabolism, glycogen, some neurotransmitters and metabolites in the citric acid cycle, and artificially introduced fluorocompounds. While hydrogen-31, phosphorus-31, carbon-13, sodium-23, and fluorine-19 in vivo results are discussed, the majority of patient studies use P-31 NMR spectroscopy. Here results from metabolic and ischemic disorders substantiate a case for spectroscopy as a diagnostic modality. The use of a broad range of spatial localization strategies is justifiable on the basis of the location and size of the pathologic condition and of NMR sensitivity. Abnormalities in spectra from many other disorders, most notably cancer, and improvements are often observed early in the course of successful therapy. Yet the potential impact of these results on clinical diagnosis and therapeutic monitoring is not always well understood, and many questions remain. Neurotransmitters and citric acid cycle metabolites exhibit high H-1 NMR sensitivities and represent major untapped potential for human clinical spectroscopy research. Studies evaluating spectroscopy in the context of existing modalities are needed. The unique ability of spectroscopy to provide noninvasive information about tissue chemistry in patients bodes well for its impact on clinical research and disease diagnosis.

The effects of surgical exposure (laminectomy) and compression trauma on various aspects of membrane lipid metabolism in the feline spinal cord were determined in this study. Tissue samples were frozen in situ and grossly dissected into gray and white portions prior to lipid analyses. Laminectomy alone resulted in measurable changes in spinal cord lipid metabolism, including increases in gray matter free fatty acids, diacylglycerols, and eicosanoids. A 90-min recovery period greatly reduced the levels of these compounds. Compression of the spinal cord with a 170-g weight (following a 90-min recovery period) caused very large increases in gray matter free fatty acids, diacylglycerols, and eicosanoids, and decreases in cholesterol and ethanolamine plasmalogens. Similar, but time delayed changes in these compounds were also observed in white matter.

Phosphatidic acid produces a selective, dose-dependent release of histamine from rat peritoneal mast cells. The effect is independent of exogenous calcium and probably reflects mobilization of sequestered stores of the cation. The significance of these results is discussed in terms of the possible changes in membrane lipid metabolism involved in mast cell activation.

There is increasing awareness that cells in culture can be a good model for studying the effects of ethanol on membrane structure and function (see Chapter by Ailing et al. in this volume). In previous studies with primary rat brain astrocytes, we have reported the effects of ethanol on morphological appearance of these cells (8). Ethanol exposure also altered the membrane lipid metabolism of these cells (17).