References: Lecithin
Fetal Diagn Ther. 1993 May-Jun;8(3):165-7.
Amniotic fluid platelet factor 4 and beta-thromboglobulin.
Saleh AA, Ozawa T, Dombrowski MP, Isada NB, Johnson MP, Evans MI, Bottoms SF, Mammen EF.
Department of Obstetrics and Gynecology, Hutzel Hospital, Wayne State University, Detroit, Mich.
Platelet activating factor (PAF), a powerful platelet activator, has been identified in human embryos and fetuses, and may induce fetal lung maturation. The potential effect of PAF on fetal platelets as indicated by release of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) has not been investigated. We measured BTG and PF4 in amniotic fluid from 78 genetic and 35 pulmonary maturity amniocenteses. BTG and PF4 were higher in the genetic amniocentesis samples (p < 0.001 in each case) than in the lung maturity samples. BTG and PF4 did not correlate with the pulmonary maturity parameters as measured by the lecithin to sphingomyelin ratio and phosphatidylglycerol concentration. Our findings suggest a fetal origin of BTG and PF4 in amniotic fluid.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8240687&dopt=Abstract lecithin
Cell Biol Toxicol. 1995 Apr;11(2):119-28.
The enzymatic removal of a surfactant coating from quartz and kaolin by P388D1 cells.
Hill CA, Wallace WE, Keane MJ, Mike PS.
National Institute of Occupational Safety and Health, Morgantown, West Virginia, USA.
The macrophage-like cell line, P388D1, was exposed to dipalmitoyl lecithin (DPL)-coated respirable quartz and kaolin, and the disappearance of the DPL was monitored for up to 9 days. The coating was removed rapidly at first (about 50% in the first 3 days) and then more slowly over the remaining 6 days, until about 30% remained on day 9. The rate of DPL digestion was independent of the type of dust and the amount of coated dust within the cell, indicating the existence of an extracellular phospholipase activity. This extracellular phospholipase activity was partially characterized. It was sensitive to temperatures above 56 degrees C, the presence of EDTA, the action of the proteases trypsin and proteinase K, and pH, being active at pH 7 but not at pH 5. This is consistent with reports in the literature of the existence of an extralysosomal phospholipase which is active at pH 7 and dependent on the presence of divalent metal ions. There was a dust-dependent difference in the extracellular rate of DPL digestion from quartz and kaolin. The coating was removed more slowly from the kaolin than it was from quartz. The removal of the DPL coating seen in the presence of cells was presumably due to both an intracellular and an extracellular phospholipase.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7583872&dopt=Abstract lecithin
Cell Biol Toxicol. 1995 Apr;11(2):79-88.
An in vitro study on the cytotoxicity of chlorhexidine digluconate to human gingival cells.
Babich H, Wurzburger BJ, Rubin YL, Sinensky MC, Blau L.
Department of Biology, Stern College for Women, Yeshiva University, New York, USA.
Chlorhexidine digluconate is the active ingredient in mouthrinses used to prevent dental plaque and gingivitis. The in vitro cytotoxicity of chlorhexidine was evaluated with the Smulow-Glickman (S-G) gingival epithelial cell line. The potency of chlorhexidine was dependent on the length of exposure and composition of the exposure medium. The midpoint cytotoxicity values for 1-, 24-, and 72-h exposures were 0.106, 0.011, and 0.0045 mmol/L, respectively. S-G cells exposed for 2 h to chlorhexidine and then maintained for 48 h in chlorhexidine-free medium were unable to recover from the initial insult. The adverse effects of chlorhexidine on the plasma membrane were suggested by the leakage of lactic acid dehydrogenase from chlorhexidine-treated S-G cells and by the increased permeability of chlorhexidine-treated liposomes to Ca2+. The toxicity of a 24-h exposure to chlorhexidine to the S-G cells was progressively lessened as the content of fetal bovine serum (FBS) in the exposure medium was increased from 2% to 8%. The potency of a 1-h exposure to chlorhexidine was reduced in medium amended with albumin, lecithin, and heat-killed Escherichia coli. These reductions in toxicity were presumably due to the binding of the cationic chlorhexidine to the negatively charged chemical moieties of the components of FBS and of albumin and lecithin and of sites on the surfaces of bacteria. Combinations of chlorhexidine and carbamide peroxide were additive in their cytotoxicities.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7583874&dopt=Abstract lecithin
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