References: Lecithin
Artif Cells Blood Substit Immobil Biotechnol. 1994;22(4):1231-6.
Perfluorodecalin emulsion tested for biocompatibility in macrophages by means of a magnetometric method.
Koester M, Lutz J, Augustin AJ, Meinert H.
Dept. of Physiology, University of Wuerzburg, Germany.
The effect of a stable perfluorodecalin (FDC) emulsion, based on addition of 0.2-0.5% (W/V) of perfluoroperhydrophenanthrene and 4% egg yolk lecithin was tested for its influence on Kupffer cells in vivo by means of a magnetometric procedure in rats. It was also compared with the effect of a perfluoro-chemical emulsion (PFC) of the first generation (FluosolR-DA, FDA). While doses of 0.1 g/kg body weight of both PFCs caused a small increase of activity in these cells (as measured by an increase in a ratio factor r after magnetization), doses of 1 g/kg b.wt. led to a significant retardation of intracellular movements after FDC and FDA for two and four days, respectively. A dose of 3 g/kg b.wt. of FDC effected a significant depression for 8 days, whereas after the same dose of Fluosol-DA the intracellular motility remained depressed for as long as 32 days.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7849927&dopt=Abstract lecithin
J Lipid Res. 1998 May;39(5):969-77.
Binding and functional effects of transcription factors Sp1 and Sp3 on the proximal human lecithin:cholesterol acyltransferase promoter.
Hoppe KL, Francone OL.
Department of Cardiovascular and Metabolic Diseases, Pfizer Inc., Groton, CT 06340, USA.
Human lecithin:cholesterol acyltransferase (LCAT) circulates in plasma bound to high density lipoproteins (HDL) and modulates the rate by which cholesteryl ester is transported to the liver. So far, little is known about the regulation of the expression of the LCAT gene. In this study we have defined the cis-elements, identified the trans-acting factors and demonstrated their functional effects and significance in determining transcriptional activity of the proximal LCAT promoter. Using deletion mutants having 5' variable ends (from nucleotides -72 to -27), we have identified the presence of two non-consensus GC-rich regions that stimulate transcription in HepG2 and HeLa cells. These regions designated sites A (-29 to -47) and B (-49 to -65) contain the CCTCC core sequence which in electromobility shift analysis is critical for the formation of two DNA-protein complexes designated I and II. Site-directed mutagenesis suggests that both sites are equally important in promoter activity, and that cooperative interactions between both sites are not required for activity. Electromobility shift and supershift experiments using oligonucleotides spanning sites A and B identified Sp1 and Sp3 as the transcription factors interacting at these sites. To determine the significance and functional effects that Sp1 and Sp3 have in regulating LCAT promoter activity, we performed transfection experiments in Drosophila SL-2 cells as they lack endogenous Sp1 and Sp3. Sp1 but not Sp3 activates the human LCAT promoter and when Sp1 is co-transfected along with Sp3, Sp3 functions as a dose-dependent repressor of Sp1-mediated activation. These findings indicate that Sp1 is capable of transactivating a reporter gene linked to the LCA
Lung. 1989;167(2):107-15.
Effect of aluminum inhalation on alveolar phospholipid profiles in experimental silicosis.
Begin R, Possmayer F, Ormseth MA, Martel M, Cantin A, Masse S.
Unite de Recherche Pulmonaire CHUS, Sherbrooke, Quebec, Canada.
In the sheep tracheal lobe model of silicosis, we have recently reported that total phospholipid, lecithin, and phosphatidylglycerol levels were elevated in lung lavage. To investigate further this observation, we obtained complete phospholipid profiles of lung lavage in 10 sheep exposed to saline only (Sa group), 10 sheep exposed to aluminum lactate inhalation only (Al group), 10 sheep exposed to 100 mg Minusil-5 in saline followed by monthly saline inhalation (Si group), and 10 sheep exposed to 100 mg Minusil-5 in saline followed by monthly aluminum lactate inhalation (Si-Al group). The following phospholipid components were measured: total phospholipids, phosphatidylglycerol (PG), phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylcholine, disaturated phosphatidylcholine, sphingomyelin, and lyso-phosphatidylcholine. All values were comparable in the Sa group, Al group, and Si-Al group. In the Si group, there was a significant increase in total phospholipid to approximately 200% of the control values. The phospholipid profile of this group demonstrated an increase in all of the phospholipid components with some enrichment of the fraction of PG, PE, and PI. We concluded that lung exposure to silica dust significantly increases the concentration of phospholipids in the alveoli. This increase is of a large spectrum of alveolar phospholipids and is completely suppressed by aluminum lactate inhalation.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2494391&dopt=Abstract lecithin
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