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PubMed1995

A comparison of the esterification of steroids by rat lecithin:cholesterol acyltransferase and acyl coenzyme A:cholesterol acyltransferase.

Although fatty acid esters of several steroids have been found in both blood and tissues, their biosynthetic origins are uncertain. For example, the fatty acid esters of delta 5-3 beta-hydroxysteroids pregnenolone and dehydroepiandrosterone (DHEA) are synthesized in tissues by an acyl coenzyme A:acyltransferase. These esters are not secreted, and the circulating esters are formed in blood by lecithin:cholesterol acyltransferase (LCAT). Fatty acid esters of corticosterone (B) and estradiol (E2) are also present in both blood and tissues, but unlike the delta 5-3 beta-hydroxysteroids, their structures are so different from cholesterol that it would not necessarily follow that they are esterified by the same enzyme. We have examined the esterification of the steroids DHEA, B, and E2 in blood and tissue, in comparison to the esterification of cholesterol, using as a model plasma and hepatic microsomes from the rat. All of the steroids were esterified in plasma, but at very different rates: cholesterol > DHEA >> E2 = B. The LCAT inhibitor, 5.5'-dithiobis-(2-nitrobenzoic acid), inhibited the esterification of all of the substrates. DHEA inhibited the esterification of cholesterol, albeit only at high concentration. The fatty acid compositions of the cholesterol and DHEA esters were analyzed, and they were found to be identical, with arachidonate the predominant ester, greater than 60%. In hepatic microsomes, the rate of esterification was different than plasma: cholesterol > E2 > or = DHEA >> B. Although B was esterified in both plasma and hepatic microsomes, the rate was exceedingly slow in both. The acyl coenzyme A:cholesterol acyltransferase inhibitor, N'-(2,4-difluorophenyl)-N-[[4-(2,2-dimethylpropyl)phenyl]- methyl]-N-heptylurea, blocked the esterification of cholesterol almost completely, but surprisingly, it had no effect on the esterification of the other steroids. The fatty acid esters of cholesterol, E2, and DHEA synthesized in the hepatic microsomes were analyzed. The composition of the cholesterol esters from the microsomes was very different than the esters of DHEA and E2. These results show that all of the steroids tested are esterified by LCAT, and consequently that blood LCAT is the probable source of the circulating steroidal esters. Most interesting are the studies of microsomal esterification. It has been presumed that similar to blood, the esterification of steroids in tissues is carried out by the same enzyme that esterifies cholesterol.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Plasma lipoproteins and lipase and lecithin:cholesterol acyltransferase activities in obese subjects before and after weight reduction.

Plasma lipoprotein concentrations and post-heparin lipoprotein lipase, hepatic triglyceride lipase (HTGL), and lecithin:cholesterol acyltransferase (LCAT) activities were determined in 10 obese women before and after weight loss. In period I, a diet was given to maintain constant weight for 3 weeks. In period II, total calories were restricted to 600 kilocalories/day for 3 weeks. In period III, caloric intake was adjusted to maintain weight at the lower level for 6 weeks. The lower calorie diet decreased plasma very low density, low density, and high density lipoprotein (HDL), cholesterol, and apolipoprotein B and A-I concentrations and molar enzyme activities, while the percent conversion of free to esterified cholesterol by the LCAT enzyme was unchanged. During weight stabilization at a lower state (period III), the mean plasma HDL cholesterol level increased, and lipoprotein lipase and LCAT activities increased to values higher than those in period I. The mean HTGL activity remained reduced. I conclude that successful weight loss improves the possibly atherogenic plasma lipoprotein profile of obese subjects. The increase in HDL cholesterol and cholesterol esterification, possibly explained by lowered HTGL enzyme activity, may increase the capacity of HDL to transport cholesterol from peripheral cells to the liver.

Adult↗
PubMed1999

Regiospecific esterification of estrogens by lecithin:cholesterol acyltransferase.

Lecithin:cholesterol acyltransferase (LCAT), the enzyme that esterifies cholesterol in blood, also esterifies other steroids at the 3beta-hydroxyl. These steroids, like cholesterol, are delta5-3beta-hydroxysteroids, such as pregnenolone and dehydroepiandrosterone. One unusual LCAT substrate is the estrogen, estradiol, which is esterified at the 17beta-hydroxyl. The esterification of estradiol by LCAT has been reported to produce a powerful antioxidant that protects low density lipoprotein (LDL) from oxidation. We investigated the substrate specificity of LCAT, comparing the esterification of four different steroids (estradiol, estriol, testosterone, and 5-androstene-3beta, 17beta-diol) by human LCAT in blood and by acyl-coenzyme A:acyltransferase in tissue (placenta and fat). Estradiol was esterified only at the D ring 17beta-hydroxyl group in both blood and tissue. In contrast, although testosterone has a D ring structure identical to that of estradiol, and it was esterified at the 17beta-hydroxyl by acyl-coenzyme A:acyltransferase in tissue, it was not esterified by LCAT. When 5-androstenediol was the substrate in the tissues, both the 3beta- and 17beta-esters were synthesized, but the major product was the 17beta-ester. Conversely, although 5-androstenediol was an excellent substrate for LCAT, only the 3beta-hydroxyl was esterified. No 17beta-ester was formed. The comparison of the esterification of estriol by acyl-coenzyme A:acyltransferase and LCAT was also surprising. In the tissues, estriol is esterified at both D ring hydroxyls, and both are esterified about equally. Although estriol is an extremely polar estrogen, it is esterified by LCAT, albeit at a very slow rate. Although again both D ring hydroxyls were esterified, the LCAT esterification site was mainly at the 17beta-hydroxyl. Esterification of estriol at the 17beta-hydroxyl in preference to the 16alpha-hydroxyl is especially striking, because the 17beta-hydroxyl group is sterically shielded by the C-18 methyl group, making esterification at this position energetically much more difficult. Furthermore, these studies demonstrate that esterification of the 17beta-hydroxyl group by LCAT is unique to estrogens. It suggests that this unusual regiospecific esterification of C-17 of the estrogens underlies a distinct stereochemical requirement for the powerful antioxidant action that has reported for the estradiol esters formed by LCAT.

Acyl Coenzyme A↗
PubMed2006

In-vitro transcutaneous delivery of ketoprofen and polyunsaturated fatty acids from a pluronic lecithin organogel vehicle containing fish oil.

This work explored the use of pluronic lecithin organogel (PLO) as a base for the delivery of bioactive polyunsaturated fatty acids from fish oil, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and ketoprofen. PLO was adapted to contain fish oil, ketoprofen, or both, and 1,8-cineole as penetration enhancer, and used to determine the in-vitro permeation from infinite and finite dosing protocols across full thickness porcine skin. Oruvail gel (2.5% ketoprofen) was included for comparison. No EPA or DHA was found to permeate skin when applied as an infinite dose. From multiple finite doses, small amount (max. 0.22%) of fish oil were found to permeate the skin. This indicates retention of fish oil within the gel matrix and that the viable domain of full thickness skin was a significant barrier. Greater amounts of EPA and DHA were delivered in the presence of ketoprofen indicating co-transport resulting from selective complexation, although no enhancement was observed using 1,8-cineole. Unlike EPA and DHA, substantial amounts of ketoprofen permeated when applied as infinite doses. Oruvail, a Carbopol 940-based hydrogel containing 2.5% ketoprofen and ethanol, delivered the greatest amount, although similar to the PLO gel containing 5% ketoprofen. The addition of propylene glycol enhanced permeation, although the presence of fish oil in the PLO gel inhibited ketoprofen permeation. When applied as multiple finite doses a maximum of 76 microm cm(-2) (1.12%) was delivered, which was reduced by the presence of 1,8-cineole. Greater permeation was again observed with Oruvail by a factor of two and with half the ketoprofen dose. To conclude, a PLO-based gel is capable of delivering EPA and DHA via a repeat finite dosing regimen, although there is evidence for the retention of these very lipophilic molecules within the gel matrix. Although to a lesser extent than EPA and DHA, ketoprofen was also substantially retained, as exemplified by the superior delivery rates from Oruvail. Finally, this work has highlighted the importance of using an appropriate topical dosing method to match the intended use of a product.

Administration, Cutaneous↗
PubMed1982

Memory decline in the aged: treatment with lecithin and physostigmine.

Normal aged subjects were given lecithin and placebo for 5 weeks each in a double-blind crossover study. Supraspan tests of memory and learning failed to show any significant changes as a result of these treatments. Addition of a single IV infusion of physostigmine did not improve performance. These findings neither support nor weaken the "cholinergic hypothesis" of cognitive impairment in aging and dementia, but they imply that simple cholinergic hypofunction is unlikely.

Acetylcholine↗
PubMed1989

Further investigations of enhancing effect of medium-chain triglycerides on d-alpha-tocopherol acetate absorption from lecithin-dispersed preparations in rat small intestine.

The effect of medium-chain triglycerides (MCTG) in lecithin-dispersed d-alpha-tocopherol acetate (VEA) preparation on intestinal absorption of VEA was investigated in rats using the in situ loop experiment. When VEA preparations containing soybean phosphatidylcholine (PC) and various amounts of MCTG were administered, the amount of VEA absorbed in 2 h was not significantly different among them. However, the amounts of total VE, sum of VEA and d-alpha-tocopherol (VE), remaining in the luminal fluid and the intestinal tissue were dependent on the MCTG content. Total VE remaining in the intestinal tissue after the administration of a VEA/PC/MCTG (5/16/1 by weight) preparation was nearly twice of VEA/PC (5/16) preparation, although the effect of MCTG varied with the increase or decrease in the MCTG content. Moreover, the increased tissue accumulation of total VE by the VEA/PC/MCTG (5/16/1) preparation resulted in an increase in the plasma VE concentration after the removal of the luminal fluid. No effect of pretreatment with PC/MCTG (1/1) dispersion on the tissue accumulation of total VE from VEA/PC (5/16) preparation was observed. Furthermore, the plasma concentration of VE from VEA and/or VE taken up in the tissue from the VEA/PC preparation was not increased by the treatment with the PC/MCTG dispersion. These results suggest that MCTG should coexist in the luminal VEA preparation to enhance the mucosal uptake. A similar enhancing effect was also observed by the addition of the metabolite of MCTG, a medium-chain fatty acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Study on absorption of indomethacin from sustained-release suppositories containing hydrogenated soybean lecithin in rabbits.

The absorption of indomethacin (IM) from suppositories containing hydrogenated soybean lecithin (HL) after rectal administration in rabbits was investigated with the aim of producing sustained-release suppositories. The suppositories were prepared by the fusion method with IM, HL and Witepsol H-15 (H-15). The IM release rate from the suppositories (IM 10 mg, HL 200 mg, total weight 1 g) was faster than that of the control suppositories without HL. The release of IM from the suppositories (IM 10 mg, HL 300 mg or 350 mg) showed slow-release profiles. In absorption studies in rabbits, sustained-plasma levels of IM were obtained when suppositories having an HL content of more than 300 mg were administered. The suppositories composed of Witepsol E-85 (melting point approximately 43 degrees C), 10 mg of IM, and 200 mg of HL, showed slow-release profiles in the release test, but did not show sustained plasma levels of IM in the absorption test. These results indicate that sustained-release suppositories able to release IM gradually from the surface of the suppositories can be obtained when HL, IM and H-15, whose melting point is lower than body temperature, are used in the preparation of the suppositories, provided that the HL content is high enough in relation to IM.

Animals↗
PubMed1991

Changes in surface charge density of lecithin liposomes by lipid peroxidation. A fluorescence study with 8-anilino-1-naphthalenesulfonate.

Treatment of lecithin liposomes with 100 microM ascorbic acid and 10 microM ferrous ion resulted in the formation of fluorescent products exhibiting an emission maximum at 430 nm and a decrease in the fluorescence intensity of 8-anilino-1-naphthalenesulfonate (ANS) bound to the liposomes without change in the emission maximum. The degree of ascorbic acid/Fe(2+)-induced decrease in the ANS fluorescence was dependent on the extent of fluorescent product formation. The results of kinetic studies on ANS-binding to the liposomes showed that treatment of the liposomes with ascorbic acid/Fe2+ causes an increase of the apparent dissociation constant (Kd) of ANS-liposome complex. This indicates that lipid peroxidation of the liposomes by treatment with ascorbic acid/Fe2+ decreases the binding affinity of ANS to the liposomes. In addition, it was also found that there is a good correlation between degrees of the Kd value and the formation of fluorescent products. The fluorescence properties, i.e. emission maximum and response of the fluorescence intensity for borohydride reduction, of the products formed by lipid peroxidation of the liposomes were similar to those derived from modification of the liposomes with monofunctional aldehydes such as acetaldehyde and heptaldehyde. From these results, it is suggested that the decrease of ANS-binding affinity to the liposomes by treatment with ascorbic acid/Fe2+ may be due to changes in the surface charge density of the liposomes relating to the formation of fluorescent products.

Anilino Naphthalenesulfonates↗
PubMed1991

Antioxidant effect of vitamin K homologues on ascorbic acid/Fe(2+)-induced lipid peroxidation of lecithin liposomes.

The effects of vitamin K homologues (K1, K2 and K3) on lipid peroxidation of lecithin liposomes induced by ascorbic acid and ferrous ion were examined. Ubiquinone-10 (UQ-10) was used as a reference in evaluation of the effectiveness of these vitamins. The lipid peroxidation was assessed by measurements of thiobarbituric acid-reactive substance (TBARS) and conjugated diene formation during the reaction. Among them, vitamins K1 and K2 inhibited the lipid peroxidation, as did UQ-10, with the order of effectiveness: UQ-10 greater than K2 greater than K1. By contrast, vitamin K3 had no inhibitory effect on ascorbic acid/Fe(2+)-induced lipid peroxidation of the liposomes. The inhibitory effect of vitamins K1 and K2 appeared only when these vitamins were incorporated into the liposomes by sonication. Simple mixing of the liposomes with these vitamins or with UQ-10 did not inhibit peroxidation of the liposomes even at high concentrations. From measurements of nitroblue tetrazolium reduction and p-nitrosodimethylaniline bleaching of vitamin K1- or K2-incorporated liposomes in the presence of ascorbic acid/Fe2+, it was found that these vitamins prevent the formation of hydroxyl radicals, not superoxide anions, during the peroxidation reaction. However, the degree of ascorbic acid/Fe(2+)-induced TBARS formation of the liposomes was not inhibited by the addition of mannitol to the reaction mixture. From these results, it is suggested that the inhibitory effect of these vitamins is mainly involved in termination of radical-chain reaction. Experimental results using several radical scavengers and/or antioxidants supported this interpretation.(ABSTRACT TRUNCATED AT 250 WORDS)

Antioxidants↗
PubMed1992

A study of the phase transition behaviours of cholesterol and saturated egg lecithin, and their interaction by differential scanning calorimetry.

The thermal behaviours of hydrogenated egg lecithin (PC) and cholesterol (C) in anhydrous form and in aqueous dispersions were studied by differential scanning calorimetry. The role of C in phase transitions of C-PC mixtures prepared by physical mixing or coprecipitating from chloroform has been examined. C underwent a phase transition at 34 degrees C and a second one at 76-78 degrees C which depended on the thermal history of the samples. C lowered the gel to liquid crystalline phase transition temperature (Tt) of the aqueous dispersions prepared from C-PC coprecipitates, broadened the endothermic peak at the Tt, and at 1:1 molar ratio the C-PC system did not undergo the phase transition. The C-PC interaction was observed below the Tt. In aqueous dispersions prepared from C-PC physical mixtures, C did not influence the phase transition and acted like an inert diluent. Pellets prepared from C-PC mixtures formed myelin bodies as a result of their erosion in 0.185 M borate buffer (pH 7.4) at below Tt, but the thermal behaviours of these myelin bodies were different for pellets prepared differently. Addition of bovine serum albumin (BSA) (10%, w/w) to the physical mixtures or coprecipitates of C-PC, or to PC alone did not show any effect on the thermal behaviours of their aqueous dispersions at the Tt.

Buffers↗
PubMed1997

Effect of additives on dissolution and swelling of soybean lecithin microcapsules prepared using the Wurster process.

Microcapsules whose membranes contained soybean lecithin (SL), cholesterol (CH), stearic acid (SA) and polyvinylpyrrolidone (PVP) at various compositions were prepared. Then, dissolution and swelling behaviors of the microcapsules in a 0.9% saline solution were studied to be related to the phase diagram of three components containing 42% of PVP in anhydrous state. In the aqueous solution, when an anhydrous microcapsule membrane was composed of SL not saturated with both CH and SA, the microcapsules showed rapid release of carbazochrome sodium sulfonate (CCSS, a model drug), poor particle-swelling and spouting of droplets containing CCSS. Long-delayed release of CCSS and drastic particle-swelling with no spouting of droplets were observed when the anhydrous membrane was composed of SL saturated with both CH and SA and the composition was not close to the two-component line, CH-SA, or to the saturation line. The spouting of droplets would be attributable to the CH and/or SA-poor SL phase and to the SL phase which dissolved CH and SA, but contained either CH or SA only in a small amount, and the delayed release would be due to the CH and SA-rich SL phase dissolving a great amount of CH and SA formed by hydration. The degree of release suppression and particle-swelling depended on the SL content. At 20-45% of SL content, the prolonged-release, great particle-swelling and no spouting of droplets at the early stage were observed only when the CH and SA-rich SL phase formed by hydration contained a high content of CH and SA.

Adrenochrome↗
PubMed1997

Effects of oral administration of soybean lecithin transphosphatidylated phosphatidylserine on impaired learning of passive avoidance in mice.

Soybean lecithin transphosphatidylated phosphatidylserine (SB-tPS) was investigated for its effect on the impaired learning of a passive avoidance task by mice induced by scopolamine or cycloheximide. SB-tPS (240, 360, 480 mg/kg) administered orally significantly prolonged the step-through latency shortened by scopolamine. SB-tPS (240 mg/kg) administered orally also prolonged the step-through latency shortened by cycloheximide. These results suggest that the effect of SB-tPS on the impaired learning behavior may be related not only to the cholinergic system but also the serotonergic system.

Administration, Oral↗
PubMed1999

Oral administration of soybean lecithin transphosphatidylated phosphatidylserine (SB-tPS) reduces ischemic damage in the gerbil hippocampus.

Mongolian gerbils orally administered with soybean lecithin transphosphatidylated phosphatidylserine (SB-tPS, 240 mg/kg) for 5 days were subjected to cerebral ischemia by bilateral common carotid artery occlusion. The pyramidal cell damage of the hippocampal CA1 subfield was classified into 4 grades according to the proportion of damaged neurons on the tenth day after the ischemic treatment. The damage score of the SB-tPS group was statistically less than that of the control group. This suggests that the pre-administration of SB-tPS may relieve the delayed neuronal cell death caused by cerebral ischemia.

Administration, Oral↗
PubMed2000

Effect of intracerebroventricular administration of soybean lecithin transphosphatidylated phosphatidylserine on scopolamine-induced amnesic mice.

The effect of intracerebroventricularly administered soybean lecithin transphosphatidylated phosphatidylserine (SB-tPS) on memory impairment was evaluated by a passive avoidance task. SB-tPS significantly prolonged the step-through latency induced by scopolamine treatment as in our previous report where SB-tPS was orally administered. The same doses of soybean phosphatidylcholine were ineffective. This result indicates that SB-tPS can act on the brain without any peripheral modification.

Amnesia↗
PubMed1996

Inhibitory effects of oxidized low-density lipoprotein on the activity of plasma lecithin: cholesterol acyltransferase.

Lecithin: cholesterol acyltransferase (LCAT) is an enzyme that is important in the cholesterol reverse-transport system by converting the surface cholesterol of high-density lipoprotein (HDL) to cholesterol ester inside HDL. We have investigated changes in plasma LCAT activity induced by oxidized low-density lipoprotein (ox-LDL). (i) LCAT activity was inhibited by the addition of even a small amount of ox-LDL, (ii) This inhibitory effect was dose-dependent and was related to the degree of oxidation of LDL, (iii) As this inhibitory effect was not prevented by antioxidants, it is suggested that it does not occur via oxidation of substrate HDL. These results suggest that cholesterol reverse-transport via HDL may be affected by ox-LDL and they are noteworthy in suggesting a new physiological function for ox-LDL.

Antioxidants↗
PubMed1998

Inhibitory effects of lipid oxidation on the activity of plasma lecithin-cholesterol acyltransferase.

We investigated the effects of free radical generation on the esterification of cholesterol by lecithin-cholesterol acyltransferase (LCAT). A water-soluble free radical initiator, 2,2'-azobis-amidinopropane dihydrochloride (AAPH), inhibited the activity of plasma LCAT as a function of the incubation time after its addition. When a small amount of oxidized HDL was added to plasma, LCAT activity was dose-dependently inhibited. To identify the effects of HDL oxidation on LCAT activity, a purified enzyme and cofactor in a vesicle solution (an artificial substrate) were used. i) LCAT activity was inhibited by the oxidation of substrate vesicles, this inhibition being related to the degree of oxidation. ii) This inhibition was observed even if apolipoprotein A-I was not oxidized. iii) Oxidized phosphatidylcholine, but not oxidized cholesterol, in the vesicles affected LCAT activity. iv) The addition of 0-40% of oxidized vesicles to normal substrate vesicles resulted in the activity of LCAT being inhibited in a dose-dependent manner. These results suggest that the esterification of cholesterol by LCAT may be affected by the oxidation of substrate phosphatidylcholine via free radical generation in the plasma.

Cholesterol↗
PubMed1999

Reduced serum lecithin:cholesterol acyltransferase activity and cholesteryl ester concentration in calves experimentally inoculated with Pasteurella haemolytica and bovine herpes virus-1.

Lecithin:cholesterol acyltransferase (LCAT), the enzyme responsible for esterification of cholesterol in plasma, is reported to be implicated in the regulation of inflammation in laboratory animals. The purpose of the present study was to elucidate the possible relevance of LCAT in the pathogenesis of calf pneumonia induced by inoculations of Pasteurella haemolytica and bovine herpes virus-1 into the calf lung. Serum LCAT activity was significantly (P < 0.01) reduced in calves inoculated with Pasteurella haemolytica. The concentration of cholesteryl esters (CE), the product of the LCAT reaction, was also decreased in the inoculated group. Decreases in LCAT activity and the CE concentration were similarly observed in calves in which bovine herpes virus-1 was inoculated. In both bacteria- and virus-inoculated calves, CE concentrations in the high-density lipoprotein fractions were distinctly decreased, whereas those in the low-density lipoprotein fractions were practically unaltered. The acute-phase proteins haptoglobin and serum amyloid A were detected in sera from the bacteria- and virus-inoculated calves; however, the two acute-phase proteins were also found in sera from the control calves. These results suggest that decreases in LCAT activity and the CE concentration are involved in the pathogenesis of pneumonia induced by inoculation of calves with Pasteurella haemolytica and bovine herpes virus-1, and also that the change in the LCAT system is more intimately related to the occurrence of calf pneumonia than the induction of acute-phase proteins such as haptoglobin.

Animals↗
PubMed2000

Reduction in serum lecithin:cholesterol acyltransferase activity prior to the occurrence of ketosis and milk fever in cows.

Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for production of cholesteryl esters in plasma. The LCAT activity is reduced in cows with fatty liver developed during the nonlactating stage and those with the fatty liver-related postparturient diseases such as ketosis. The purpose of the present study was to examine whether reduced LCAT activity during the nonlactating stage could be detected before the occurrence of postparturient diseases. Sera from 24 cows were collected at approximately 10-day intervals from -48 to +14 days from parturition. Of the 24 cows, 14 were apparently healthy, whereas 7 had ketosis and 3 had milk fever at around parturition. Of the 14 healthy cows, 7 had unaltered LCAT activity during the observation period, whereas 7 showed reduced activity from -20 to +14 days. Ketosis and milk fever occurred at from -3 to +10 days, but reductions of LCAT activity in diseased cows had already been observed from days -20 to 0. These results suggest that LCAT activity is virtually unaffected during the peripartum period at least in some healthy cows and also that the reduction in LCAT activity can be detected before the occurrence of ketosis and milk fever.

Animals↗