Lipid inhibition

Civoli F, Daniel LW (1998) Quaternary ammonium analogs of ether lipids inhibit the activation of protein kinase C and the growth of human leukemia cell lines. Cancer Chemother Pharmacol 42 319-326... 

Similarly to their antibacterial activity, resorcinolic lipids exhibit fungistatic properties. However, experiments indicate that resorcinolic lipids inhibit the growth of Trichophyton mentagrophytes and Saccharomyces cerevisiae to a lower degree than observed for bacteria. No activity was shown against Candida albicans and Asperigullus niger [256]. The occurrence of 5-n-(heptadec-12-enyl) and 5-n-... 

The lack of involvement of photosynthetic inhibitions in lipid inhibitions by pyridazinones is also supported by results in non-photosynthetic tissue (11, 12). The phospholipids predominate in root membranes. The data in Table V show that BASF 13 338 does not influence the distribution of lipid between the various classes of phospholipids, but BASF 13 338 specifically decreases the linolenic acid content of phosphatidylcholine and phosphatidylethanolamine. 

First, the peroxyl radical abstracts a hydrogen atom from the phenolic antioxidant to yield a hydroperoxide and aroxyl radical that subsequently undergoes radical coupling to give peroxide products. The rate of oxidation of a lipid inhibited by a phenolic antioxidant requires consideration of the following reactions too ... 

Foldes-Filep E, Sirois P, Filep JG. Pulmonary surfactant lipids inhibit prostanoid production of guinea pig alveolar macrophages. J Leukoc Biol 1994 56 475-480. 

Following the action of extraordinary stimulants (hypoxic hypoxia, hypoxia + hyperoxia, hypodynamia + hyperthermia), animals demonstrate an accumulation of malonic dialdehyde with a simultaneous fall of antiradical activity of the liver tissue. A preliminary introduction to rats of acetylene amine 3,4,5-tris(morpho-linopropynyl)-l-methylpyrazole 103 and also of tocopherol antioxidant and gutumine antihypoxant averts activation of the lipid peroxidation processes. The inhibition of peroxidation with this agent is mediated by stabilization of ly-zosomal and mitochondrial membranes. Unsaturated amines prevent destruction of the organelle membranes provoked by UV irradiation and incubation at 37°C (pH4.7)(78MIl). 

The acetylene aminopyrazole 103 was capable of inhibiting the processes of lipid peroxidation both in the enzymatic and nonenzymatic peroxidation system (76MI2). Finally, 4-[3-(l-methyl-l//-pyrazol-3-yl)-prop-2-ynyl]morpholine hydrochloride 104 was patented as a compound with high hypoxic activity (93MIP1). 

Viruses are small infectious agents composed of a nucleic acid genome (DNA or RNA) encased by structural proteins and in some cases a lipid envelope. They are the causative agents of a number of human infectious diseases, the most important for public health today being acquired immunodeficiency syndrome (AIDS), hepatitis, influenza, measles, and vituses causing diarrhoea (e.g., rotavirus). In addition, certain viruses contribute to the development of cancer. Antiviral drugs inhibit viral replication by specifically targeting viral enzymes or functions and are used to treat specific virus-associated diseases. 

The antiinflammatory effects of statins likely result from their ability to inhibit the formation of mevalonic acid. Downstream products of this molecule include not only the end product, cholesterol, but also several isoprenoid intermediates that covalently modify ( pre-nylate ) certain key intracellular signaling molecules. Statin treatment reduces leukocyte adhesion, accumulation of macrophages, MMPs, tissue factor, and other proinflammatory mediators. By acting on the MHC class II transactivator (CIITA), statins also interfere with antigen presentation and subsequent T-cell activation. Statin treatment can also limit platelet activation in some assays as well. All these results support the concept that in addition to their favorable effect on the lipid profile, statins can also exert an array of antiinflammatory and immunomodulatory actions. 

The blood-brain barrier (BBB) forms a physiological barrier between the central nervous system and the blood circulation. It consists of glial cells and a special species of endothelial cells, which form tight junctions between each other thereby inhibiting paracellular transport. In addition, the endothelial cells of the BBB express a variety of ABC-transporters to protect the brain tissue against toxic metabolites and xenobiotics. The BBB is permeable to water, glucose, sodium chloride and non-ionised lipid-soluble molecules but large molecules such as peptides as well as many polar substances do not readily permeate the battier. 

In vitro and ex vivo studies have shown that FATPs transport LCFAs and very long-chain fatty acids (VLCFAs) but no medium-chain fatty acids, fatty acid esters, or lipid-soluble vitamins [4]. LCFA transport is inhibited by prior protease treatment. Synthetic substrates for FATPs include 14C-labeled fatty acids and the fluorescently labeled fatty acid analogue C1 -BODEP Y-Cl 2. Using the latter substrate, differences in fatty acid uptake kinetics between FATP expressing 3T3 LI adipocytes and 3T3 LI fibroblasts, which are devoid of FATPs, can be readily appreciated (Fig. 2). 

Phloretin inhibits FATP-mediated traversing of fatty acids across lipid bilayers. Phloretin is the aglycon of phlorizin and has been used to terminate the uptake of LCFAs and VLCFAs in timed in vitro uptake assays with cultured cells or in ex vivo uptake assays with isolated primary cells. 

Increased lipid synthesis/inhibi-tion of lipolysis Activation of lipoprotein lipase (LPL)/induc-tion of fatty acid synthase (FAS)/inactivation of hormone sensitive lipase (HSL) Facilitated uptake of fatty acids by LPL-dependent hydrolysis of triacylglycerol from circulating lipoproteins. Increased lipid synthesis through Akt-mediated FAS-expression. Inhibition of lipolysis by preventing cAMP-dependent activation of HSL (insulin-dependent activation of phosphodiesterases )... 

Na+-dependent inactivation. There is a sequence of 20-aminoacids (219-23 8), located in the intracellular f loop near the membrane lipid interface, that seems to be involved in the Na+-dependent inactivation. This autoinhibitory 20-aminoacid sequence might interact with another portion of the f loop (562-679) producing NCX inhibition. In accordance with this view, the synthetic peptide provided with the same sequence of XIP region blocks NCX activity. 

Prostaglandins are a group of lipid autacoids known as eicosanoids. They are produced from membrane phospholipids and found in almost every tissue and body fluid. They are involved in a number of physiological processes including inflammation, smooth muscle tone and gastrointestinal secretion. In the central nervous system they have been reported to produce both excitation and inhibition of neuronal activity. 

OGR1, but not GPR4 or TDAG8, is sensitive to inhibition by zinc and copper ions [1]. Agonistic or antagonistic modulators of receptor function are not yet published As described above, we do not consider lipid messengers as specific modulators of these receptors. 

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