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PubMed1999

Effects of smoking on serum lipid and lipoprotein concentrations and lecithin: cholesterol acyltransferase activity.

Cigarette smoking is one of the major risk factors for cardiovascular disease. The mechanism responsible for this association is still unknown. We measured the activity of lecithin: cholesterol acyltransferase (LCAT), a key factor in the esterification of plasma cholesterol and reverse cholesterol transport, and the levels of lipids and apolipoproteins in the serum of 27 cigarette smoking and 31 non-smoking (control) men. We could not find any significant difference among these parameters between the groups. Serum LCAT activity was lower in smokers, but the difference was statistically nonsignificant. We also classified the two groups in respect to their serum lipid levels as hyper- and normolipidemic, we observed that normolipidemic-smokers had lower (p < 0.05) high density lipoprotein-cholesterol (HDL-C) and HDL-ester cholesterol levels compared to the normolipidemic-nonsmokers. While there were no any significant differences between hyperlipidemic-smokers and nonsmokers with respect to any of the parameters. In the end we have got the idea that smoking seems to affect HDL-C and HDL-ester cholesterol levels in the normolipidemic-smokers group, only, Also, LCAT activity tended to be lower in smokers compared to nonsmokers.

Adult↗
PubMed2000

Phosphatidylcholine fluidity and structure affect lecithin:cholesterol acyltransferase activity.

The purpose of this study was to test the hypothesis that lipid fluidity regulates lecithin:cholesterol acyltransferase (LCAT) activity. Phosphatidylcholine (PC) species were synthesized that varied in fluidity by changing the number, type (cis vs. trans), or position of the double bonds in 18 or 20 carbon sn-2 fatty acyl chains and recombined with [(3)H]cholesterol and apolipoprotein A-I to form recombinant high density lipoprotein (rHDL) substrate particles. The activity of purified human plasma LCAT decreased with PC sn-2 fatty acyl chains containing trans versus cis double bonds and as double bonds were moved towards the methyl terminus of the sn-2 fatty acyl chain. The decrease in LCAT activity was significantly correlated with a decrease in rHDL fluidity (measured by diphenylhexatriene fluorescence polarization) for PC species containing 18 carbon (r(2) = 0.61, n = 18) and 20 carbon (r(2) = 0.93, n = 5) sn-2 fatty acyl chains. rHDL were also made containing 10% of the 18 carbon sn-2 fatty acyl chain PC species and 90% of an inert PC ether matrix (sn-1 18:1, sn-2 16:0 PC ether) to normalize rHDL fluidity. Even though fluidity was similar among the PC ether-containing rHDL, the order of PC reactivity with LCAT was significantly correlated (r(2) = 0.71) with that of 100% PC rHDL containing the same 18 carbon sn-2 fatty acyl chain species, suggesting that PC structure in the active site of LCAT determines reactivity in the absence of measurable differences in bilayer fluidity. We conclude that PC fluidity and structure are major regulators of LCAT activity when fatty acyl chain length is constant.

Apolipoprotein A-I↗
PubMed2000

Relationship between structure and biochemical phenotype of lecithin:cholesterol acyltransferase (LCAT) mutants causing fish-eye disease.

In order to test the hypothesis that fish-eye disease (FED) is due to a deficient activation of lecithin:cholesterol acyltransferase (LCAT) by its co-factor apolipoprotein (apo) A-I, we overexpressed the natural mutants T123I, N131D, N391S, and other engineered mutants in Cos-1 cells. Esterase activity was measured on a monomeric phospholipid enelogue, phospholipase A(2) activity was measured on reconstituted high density lipoprotein (HDL), and acyltransferase activity was measured both on rHDL and on low density lipoprotein (LDL). The natural FED mutants have decreased phospholipase A(2) activity on rHDL, which accounts for the decreased acyltransferase activity previously reported. All mutants engineered at positions 131 and 391 had decreased esterase activity on a monomeric substrate and decreased acyltransferase activity on LDL. In contrast, mutations at position 123 preserved these activities and specifically decreased phospholipase A(2) and acyltransferase activites on rHDL. Mutations of hydrophilic residues in amphipathic helices alpha 3;-4 and alpha His to an alanine did not affect the mutants' activity on rHDL. Based upon the 3D model built for human LCAT, we designed a new mutant F382A, which had a biochemical phenotype similar to the natural T123I FED mutant. These data suggest that residues T123 and F382, located N-terminal of helices alpha 3-4 and alpha His, contribute specifically to the interaction of LCAT with HDL and possibly with its co-factor apoA-I. Residues N131 and N391 seem critical for the optimal orientation of the two amphipathic helices necessary for the recognition of a lipoprotein substrate by the enzyme.

Animals↗
PubMed2000

Effect of growth hormone replacement therapy on plasma lecithin:cholesterol acyltransferase and lipid transfer protein activities in growth hormone-deficient adults.

The effects of growth hormone (GH) replacement on plasma lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP), and phospholipid transfer protein (PLTP), factors involved in high density lipoprotein (HDL) metabolism, are unknown. We carried out a 6 months study in 24 GH-deficient adults who were randomized to placebo (n = 8), low dose GH (1 U daily, n = 8), and high dose GH (2 U daily, n = 8), followed by a 6 months open extension study with high dose GH (1 drop-out). No significant changes in plasma lipoproteins, LCAT, CETP, and PLTP activities, cholesterol esterification (EST) and cholesteryl ester transfer (CET) were observed after placebo. After 6 months of GH (combined data, n = 24), very low + low density lipoprotein (VLDL + LDL) cholesterol (P < 0.05) and apolipoprotein B (P < 0.05) decreased, whereas HDL cholesterol and HDL cholesteryl ester increased (P < 0. 05). Prolonged treatment showed comparable effects. Plasma apolipoprotein A-I and Lp[a] remained unchanged. Plasma LCAT (P < 0. 01) and CETP activities (P < 0.01), as well as EST (P < 0.01) and CET decreased (P < 0.01) after 12 months of GH (n = 15), but PLTP activity did not significantly change. Changes in EST and CET after 12 months of treatment were independently related to changes in plasma LCAT (P = 0.001 and CETP activity (P = 0.01). In conclusion, GH replacement therapy improves the lipoprotein profile in GH-deficient adults. Chronic GH replacement lowers plasma LCAT and CETP activities, contributing to a decrease in cholesterol esterification and cholesteryl ester transfer. These effects may have consequences for HDL metabolism and reverse cholesterol transport.

Adult↗
PubMed2000

Anti-goitrous effect of lecithin-bound iodine in propylthiouracil treated rats.

OBJECTIVE: Excess iodine and some iodine-containing compounds are known to affect various parameters of thyroid function. Lecithin-bound iodine (LBI) is a compound which induces involution of an enlarged thyroid. LBI was tested for its ability to affect thyroid ornithine decarboxylase (ODC) activity and apoptosis. METHODS: LBI was given orally to propylthiouracil-pretreated rats and the changes in ODC activity and apoptosis were observed. The thyroid apoptosis was detected by DNA laddering and flow cytometry. RESULTS: LBI suppressed the thyroid ODC activity within one hour after its administration and lowered slightly but significantly the thyroid putrescine levels at 3 h. The DNA cleavage ladder was evident at 3-6 h after LBI treatment. Propylthiouracil induced thyroid enlargement was reduced significantly at 3 days after chronic treatment with LBI. The thyroidal content of putrescine was also decreased after chronic treatment. These effects of LBI were essentially the same as those of excess iodide, while other iodinated compounds including amiodarone, iopanoic acid and erythrosine had no effect on the thyroid ODC activity. CONCLUSIONS: These results suggest that LBI may exert its anti-goitrous effects, consisting of the inhibition of ODC activity and apoptosis, in the form of inorganic iodide in vivo.

Animals↗
PubMed2000

Lecithin:retinol acyltransferase from mouse and rat liver. CDNA cloning and liver-specific regulation by dietary vitamin a and retinoic acid.

Lecithin:retinol acyltransferase (LRAT), present in microsomes, catalyzes the transfer of the sn-1 fatty acid of phosphatidylcholine to retinol bound to a cellular retinol-binding protein. In the present study we have cloned mouse and rat liver LRAT cDNA and tested the hypothesis that LRAT mRNA, like LRAT activity, is regulated physiologically in a liver-specific manner. The nucleotide sequences of mouse and rat liver LRAT cDNA each encode a 231-amino acid protein with 94% similarity between these species, and approximately 80% similarity to a cDNA for LRAT from human retinal pigment epithelium. Expression of rat LRAT cDNA in HEK293T cells resulted in functional retinol esterification and storage. RNA from several rat tissues hybridized with liver LRAT cDNA. However, LRAT mRNA was virtually absent from the liver of vitamin A-deficient animals, while being unaffected in intestine and testis. LRAT mRNA was rapidly induced by retinoic acid (RA) in liver of vitamin A-deficient mice and rats (P < 0.01). LRAT mRNA and enzymatic activity were well correlated in the same livers of rats treated with exogenous RA (r = 0.895, P < 0.0001), and in a dietary study that encompassed a broad range of vitamin A exposure (r = 0.799, P < 0.0001). Liver total retinol of <100 nmol/g was associated with low LRAT expression (<33% of control). We propose that RA, derived exogenously or from metabolism, serves as an important signal of vitamin A status. The constitutive expression of liver LRAT during retinoid sufficiency would serve to divert retinol into storage pools, while the curtailment of LRAT expression in retinoid deficiency would maintain retinol for secretion and delivery to peripheral tissues.

Acyltransferases↗
PubMed2000

[Transdermal delivery mechanisms of lecithin nanoparticles with cyclosporin A through mice skin].

AIM: To investigate the transdermal delivery mechanisms of the flexible nano-liposomes, conventional nano-liposomes and lecithin-cholate mixed micelles through mouse skin. METHODS: Liposomes and micelles were applied onto the mouse skin non-occlusively in vitro and in vivo, then the drug concentrations in the skin, receiver and blood were determined. RESULTS: In vitro permeation studies showed that flexible nano-liposomes and mixed micelles transported measurable amount of cyclosporin A through the skin. Conventional liposomes precluded drugs permeate through the skin while deposited it in the skin. In vivo studies indicated that blood concentration reached peak value at 8 h after the application of flexible nano-liposomes. Both conventional nano-liposomes and mixed micelles failed to deliver measurable amount of drug into the blood. CONCLUSION: Liposomes fuse with the skin. Flexible nano-liposomes penetrate through the skin under the pressure of hydration force. Mixed micelles promote transfer in state of solution.

Administration, Cutaneous↗
PubMed2001

Solubilization of bromhexine hydrochloride in aqueous lecithin dispersions. Physicochemical characterization of interactions between drug and carrier.

In aqueous systems bromhexine hydrochloride (Br-HCl) has a poor solubility (4.54 mg/g) and displays no amphiphilic character e.g. self association. Therefore the drug is molecularly dispersed in water until the solubility product of Br-HCl is exceeded. Solubilization of Br-HCl is linearly increased on addition of lecithin; calculations show that 10 mg Phospholipon 90G (P 90G) enable solubilization of additional 1.25 mg Br-HCl after the solubility product of Br-HCl has been exceeded. This means that four to five phospholipid molecules are needed for the solubilization of one drug molecule. Ternary systems with P 90G concentrations up to 20% have a lamellar microstructure. The systems are multilamellar vesicle dispersions as polarisation microscopy, transmission electron microscopy and small-angle X-ray diffractometry suggest. Furthermore, Br-HCl solubilization leads to a significant reduction of the interlamellar distance d and increases the elastic properties of the systems. 31P NMR data provide evidence that Br-HCl is solubilized within the lipophilic part of the phospholipid bilayer.

Bromhexine↗
PubMed1975

Effect of aerosolized dipalmitoyl lecithin on oxygen-toxic rat lungs.

Pulmonary surfactant is reduced in oxygen toxicity but whether this represents a decrease in production or inactivation of surface-active material already present is not known. We divided 200 g male Wister-Lewis rats into different experimental groups. The animals were exposed continuously to 0, 48, 56 or 72 h of close to 100% oxygen at atmospheric pressure. Administration of aerosolized dipalmitoyl lecithin (DPL) in phosphate buffer had no effect on lung deflation compliances or lung stability indices of any group. Exposure to DPL by spontaneous respiration and/or controlled ventilation made no difference. Lung dry/wet weight ratios fell in animals exposed to aerosols of DPL + buffer + O2, buffer + O2, or water + O2, to aerosols of DPL + buffer + O2, buffer + O2, or water + O2, as compared to animals with similar lengths of oxygen exposure not exposed to an aerosol. If the initial pulmonary pathophysiological response to 100% oxygen at 1 atm pressure is capillary logical response to 100% oxygen at 1 atm pressure is capillary endothelial damage with leakage of intravascular fluids into the alveoli, then exogenously administered DPL would not be of benefit in pulmonary oxygen toxicity. Our study suggests that aerosolized DPL administered to normal animals and animals exposed to oxygen for 48-72 h had no effect on lung compliance or stability.

Aerosols↗
PubMed1975

A simplified procedure for synthesis of di-[14C]acyl-labeled lecithins.

A simplified procedure for synthesis of 1,2-di-[1'-14C]oleoyl-, 1,2-di-[1'-14C]linoleoyl-, and 1,2-di-[1'-14C]eicosatrienoyl-sn-glycero-3-phosphorylcholine is described. The method involves acylation of the CdCl2 complex of glycerophosphorylcholine with a 14C-labeled fatty acid in the presence of trifluoracetic anhydride and pyridine. The 14C-labeled lecithin is isolated in pure form by preparative thin-layer chromatography and alumina column chromatography in an overall yield of 12-24%. No isomerization or peroxidation of the unsaturated acids was detected.

Carbon Radioisotopes↗
PubMed1999

[Effect of Astragalus Angelica Mixture on lipoprotein lipase and lecithin cholesterol acyltransferase of nephrotic rats].

OBJECTIVE: To investigate the mechanism of Astragalus Angelica Mixture (AAM) effect of regulating lipid metabolism disturbance in nephrotic rats. METHODS: To examine the effects of AAM on serum albumin, lipid levels, and activities of lipoprotein lipase (LPL) and lecithin-cholesterol acyltransferase (LCAT), which are key enzymes for catabolism of lipid, in immune-induced nephrotic hyperlipidemia rats and exogenous hyperlipidemia rats. RESULTS: Serum albumin was reduced, lipid increased significantly, LPL activity decreased significantly and the LCAT activity was relatively insufficient in nephrotic rats. Activities of LPL and LCAT increased significantly in AAM treated nephrotic rats. There were no change of activities of LPL and LCAT in exogenous hyperlipidemia rats and AAM showed no effect on the activities of these two enzymes. CONCLUSION: The effect of AAM in regulating lipid metabolism might be due to enhancing the clearance of triglyceride and cholesterol-rich lipoprotein by improving the activities of LPL and LCAT.

Animals↗
PubMedDate not supplied

Lecithin: cholesterol acyltransfer, dyslipoproteinaemia and membrane lipids in uraemia.

BACKGROUND: Dyslipoproteinaemia is the most important complication linked to the increased morbidity and mortality of uraemic patients from cardiovascular disease. Many factors contribute to the dyslipoproteinaemia, including increased production of very low density lipoproteins (VLDL), decreased lipolysis and impaired low density lipoprotein (LDL) receptor activity. In this study, the role of decreased lecithin:cholesterol acyltransferase (LCAT) activity in relation to plasma and membrane lipid changes is examined. METHODS: Fasted blood samples were taken from 65 uraemic patients, including roughly equal numbers of haemodialysis, peritoneal dialysis and undialysed subjects, and from 29 apparently healthy individuals. Plasma total and free cholesterol, cholesteryl esters (CE), total and individual phospholipids, high density lipoprotein (HDL)-, LDL- and VLDL-cholesterol were all measured, as were erythrocyte and lymphocyte free cholesterol and phospholipids. RESULTS: More than half of all patients, including those both on haemodialysis and peritoneal dialysis, as well as untreated individuals, had relative plasma concentrations of CE below the normal mean - 2SD. These patients had significantly decreased LDL- (2.62 +/- 1.04 compared to 3.61 +/- 0.97 mmol/L; p < 0.001) and HDL-cholesterol (0.71 +/- 0.30 compared to 0.94 +/- 0.27 mmol/L; p < 0.01) and increased VLDL-cholesterol (0.60 +/- 0.50 compared to 0.47 +/- 0.26 mmol/L; p < 0.05) as well as significant increases in membrane cholesterol and cholesterol/phospholipid molar ratio in erythrocytes (3.30 +/- 0.49 and 0.87 +/- 0.08 compared to 2.95 +/- 0.18 mmol/g wet weight and 0.76 +/- 0.04 mol/mol respectively, both p < 0.001) and cholesterol/phospholipid molar ratio of lymphocytes (0.58 +/- 0.14 compared to 0.45 +/- 0.04 mol/mol; p < 0.001). They were markedly deficient in LCAT activity (56.1 +/- 20.4 compared to 105.5 +/- 17.5 nmol/ml/h; p < 0.001). The LCAT activity in plasma of patients with high CE was higher than for those with low CE, but it was also significantly less than normal and this group showed smaller changes in other lipid parameters. CONCLUSIONS: LCAT deficiency is common in uraemia and is associated with changes not just in plasma lipids, but also in membrane lipids which may be relevant to the progression of the disease.

Adult↗
PubMed2002

Retinol metabolism and lecithin:retinol acyltransferase levels are reduced in cultured human prostate cancer cells and tissue specimens.

Recent studies from our laboratory have indicated that the metabolism of vitamin A (retinol) to retinyl esters, carried out primarily by the enzyme lecithin:retinol acyltransferase (LRAT), is greatly reduced in human carcinoma cell lines of the oral cavity, skin, breast, and kidney as compared with their normal epithelial counterparts. These studies suggest that human carcinoma cells are retinoid-deficient relative to normal epithelial cells. In this study, we examined the metabolism of [(3)H]retinol and [(3)H]retinoic acid (RA) in human prostate cancer lines and in primary cultures of human prostate epithelial cells. Normal cells esterified all of the [(3)H]retinol added to the cultures. In contrast, all seven prostate cancer cell lines and four primary cultures derived from prostatic adenocarcinomas metabolized only trace amounts of [(3)H]retinol to [(3)H]retinyl esters. Correlated with this relative lack of esterification of [(3)H]retinol by the cancer cells was loss of expression of LRAT protein, whereas normal cells expressed abundant levels of LRAT protein by Western analysis. The metabolism of [(3)H]RA was also examined in these prostatic cells. Two of the prostate cancer tumor lines, DU 145 and PJ-1, exhibited rapid metabolism of [(3)H]RA; in contrast, the other tumor lines or primary cultures metabolized [(3)H]RA at a much slower rate. We also found that the immortalization of normal human prostatic epithelial cells by SV40 T antigen led to a reduction in LRAT protein expression and esterification of [(3)H]retinol. Further transformation to tumorigenicity with the ras oncogene resulted in loss of detectable LRAT expression. Finally, we analyzed LRAT protein expression in tissue sections from six prostatectomy specimens by immunohistochemistry. LRAT protein was predominantly expressed in the basal cells of normal prostatic epithelium, whereas its expression was lost in prostate cancer. Collectively, these data implicate aberrant retinoid metabolism in the process of prostatic carcinogenesis.

Acyltransferases↗
PubMed2002

[Expression of lecithin cholesterol acyltransferase and/or apoA-I mediated by recombinant adeno-associated virus in myogenic cells].

Lecithin cholesterol acyltransferase (LCAT) is the major enzyme producing most plasma cholesterol esters(CE) and a key participant in the process of reverse cholesterol transfer (RCT). The aim of this research is to co-express LCAT and it's natural activator apoA-I, with the recombinant adeno-associated virus vectors in the skeletal muscle cells, in order to pave a new way for gene therapy of the primary or secondary LCAT deficiency. 293T cells was cotransfected with pDG and rAAVAIL/rAAVL plasmids to produce infectious rAAV, and non-ionic iodixanol gradient centrifugation, followed by heparin affinity chromatography, were performed for separation, purification and concentration of rAAV. The particle numbers of rAAV, assayed by dot blot, were 7 x 10(14)/L (rAAVAIL) and 1 x 10(14)/L (rAAVL). These vectors were then transduced into C2C12 myoblasts. The results of ELISA and Western blot for human apoA-I, and [3H]-cholesterol-labeled radiochemical methods for LCAT activity, showed that the expression of human apoA-I cDNA and/or human LCAT cDNA in transduced C2C12 cells lasted for 30 days, even after myoblasts were differentiated into myotubes. PCR products for the transgene indicated the long-term persistence of transduced vector sequences. The results indicate that the methods used for production and purification of rAAV is efficient, and rAAV vector mediated the expression and secretion of LCAT and apoA-I gene in C2C12 myoblasts successfully. It suggests that the use of rAAV vectors mediating the high efficiency, long-term expression of human LCAT cDNA and/or apoA-I cDNA in skeletal muscle in vivo can be a safe and fesible strategy for the gene therapy of LCAT deficiency.

Animals↗
PubMed1975

Evaluation of an in vitro assay of lecithin:cholesterol acyl transfer rate in plasma.

Crucial and previously criticized points in a slightly modified version of the Stokke-Norum assay of fractional lecithin:cholesterol acyl transfer (LACT) rate in plasma were studied. LCAT activity in the albumin added to the assay medium and negative influence of remaining organic solvent were important sources of error that it was necessary to eliminate. The assumption of equilibration of labeled cholesterol among lipoproteins in vitro was supported experimentally. Addition of isolated chylomicrons had no influence on initial LACT rate. Incubation time was decreased to 20 minutes to obtain a better estimate of initial LCAT rate in normals. Using gas-liquid chromatography to determine unesterified cholesterol concentration, the precision of measurement of molar LCAT rate was 5.2 per cent (coefficient of variation). Molar LCAT rate in healthy males 20-60 years of age was 56-130 mumol-1(-1)-h-1 (mean +/- 2 S.D.) and compared well with reports from other laboratories and in vivo measurements. At present this methodology is considered to be suitable for studies of LCAT and cholesterol turnover in different metabolic situations and clinical materials.

Acetone↗
PubMed2002

Decreased laboratory testing for lecithin-to-sphingomyelin ratio and phosphatidylglycerol after fetal lung maturity assessment from lamellar body count in amniotic fluid.

The objectives of this study were to do inexpensive lamellar body count (LBC) in amniotic fluid, to do statistical analysis to evaluate cutoff values for fetal lung maturity (FLM) and fetal lung immaturity (FLI), to derive a threshold for obtaining a lecithin-to-sphingomyelin (L/S) ratio and phosphatidylglycerol percentage (%PG), and to determine the potential cost savings to the hospital if they use this new method. Testing (LBC, L/S ratio, and %PG) was done on 123 specimens of amniotic fluid. Receiver operating characteristic (ROC) curve, discriminant, linear regression, chi2, and cost analyses were used to evaluate the laboratory and financial parameters. Lamellar body counts of greater than 41,500 (Coulter MAXM: sensitivity, 90.5%; specificity, 87.7%; positive predictive value, 79.2%; negative predictive value, 94.7%) and greater than 32,000 (Coulter Gen.S: sensitivity, 90.5%; specificity, 85.2%; positive predictive value, 76.0%; negative predictive value, 94.5%) were the best threshold for biochemical FLM. Similarly, LBC of less than 24,000 (MAXM: sensitivity, 78.6%; specificity, 100%; positive predictive value, 100%; negative predictive value, 90.0%) and less than 21,000 (Gen.S: sensitivity, 71.4%; specificity, 100%; positive predictive value, 100%; negative predictive value, 87.1%) provided the best statistical cutoff for biochemical FLI from discriminant analysis. The authors concluded that FLM and FLI can be predicted with reasonable accuracy from LBC in amniotic fluid specimens. The expensive and not easily accessible L/S ratio and %PG can then be done only in cases in which LBC indicates transitional FLM. A cascade approach results in 86% savings to the hospital if the L/S ratio and %PG are not sent to a reference laboratory.

Adult↗
PubMedDate not supplied

[The lecithin-sphynogomyelin ratio in the amniotic fluid in insulin dependent diabetic pregnancies].

A delay in the pulmonary maturation of the foetus of diabetic mothers assessed by the lecithin-sphingomyelin (L/S) ratio has been reported (2, 3, 5). A suggestion has been raised that the results of the L/S ratio should be viewed with caution in predicting lung maturity in pregnancies complicated by maternal diabetes (8). We report our findings on 52 insulin-dependent diabetic pregnancies which involved 90 estimations of the L/S ratio on the amniotic fluid. In all cases, the L/S ratio accurately reflected lung maturity, as no hyaline membrane disease (HMD) was observed with a L/S ratio greater than 2. There was no significant difference in the proportion of mature fetal lung between insulin-dependent diabetics and controls for each week of pregnancy between 32 and 38 weeks. There is no statistical difference in the mature L/S ratio between classes B + C and D + F diabetics.

Amniotic Fluid↗
PubMed1975

Effect of ozone exposure on lecithin : cholesterol acyltransferase activity in rat serum.

Studies are reported here of relationships of ozone exposure and lecithin : cholesterol acyltransferase (LCAT) activity in rat serum. Exposure to low concentrations of ozone (1.1+/-0.27 ppm) for 24 hrs, significantly elevated LCAT activity, while the concentration of free cholesterol in rat serum was little changed during the exposure. In contrast, LCAT activity was decreased by exposure to high concentrations of ozone (2.0-2.5 ppm) for 24 hrs.

Acyltransferases↗