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PubMed1979

Lecithin changes in murine Mycoplasma pulmonis respiratory infection.

We examined the lipid content of bronchoalveolar (BA) washes from both mice and rats infected with Mycoplasma pulmonis, an etiological agent of murine pneumonia. During a 30-day period after intranasal inoculation, the total lipid content from infected and control rats (in milligrams per animal) remained relatively equal and unchanged. The saturated, unsaturated, and total lecithin contents in infected rats (in milligrams per animal) all increased. The maximum lecithin values were detected at 7 to 10 days after infection; later, the levels fell to control values. There was essentially no change in any lecithin value from uninfected animals. Although in BA washes from infected animals the mass of disaturated lecithins increased, the percentage of this fraction in the total lecithin pool decreased. The fatty acids of the lecithins from BA washes of infected mice had significantly less palmitic and significantly more oleic and linoleic acids than the lecithins isolated from the BA washes of control animals. Both the relative decrease in the mass of disaturated lecithins in the BA washes and the increase in the percentage of esterified unsaturated fatty acids in the lecithins may be directly related to the reduced lung function reported to occur during the course of murine M. pulmonis pneumonia.

Animals↗
PubMed1975

Recirculation and reutilization of micellar bile lecithin.

Bile lecithins, solubilized in micellar bile salt and radiolabeled in the 1-acyl fatty acid, phosphorus, and choline positions, were infused in the small bowel of fasted rats. Absorption of each label was virtually complete after 24 h. However, these lecithins were extensively hydrolyzed in the bowel lumen as well as after absorption, and neither the fatty acid nor phosphorus was significantly retained in the enterohepatic circulation or reutilized for biliary lecithin synthesis. In contrast, while choline was also dissociated from absorbed lecithin, choline was instead retained in the liver, reincorporated into newly synthesized hepatic lecithin, and sercreted in biliary lecithin in 10-fold greater amounts than either the fatty acid or phosphorus. However, the extent of choline incorporation into bile lecithin was limited and was not further increased when free choline was directly injected into the portal vein. The data therefore suggest that although only choline of absorbed lecithin is retained in the enterohepatic circulation and preserved for new biliary lecithin synthesis, exogenous choline utilization is regulated by the size of the available hepatic pool.

Animals↗
PubMed1976

Estimation of surfactant lecithin in amniotic fluid and prediction of respiratory distress syndrome.

The quantitative and qualitative analyses of lecithin in the human amniotic fluid in relation to the antenatal prediction of developing respiratory distress syndrome were described. Surfactant lecithin (disaturated and/or dipalmitoyl lecithin) was estimated for the first time in 42 amniotic fluid specimens of 21-42 weeks gestation. Surfactant lecithin was present in considerable amounts in specimens obtained near or at term except in the ones associated with infants who subsequently developed respiratory distress syndrome. One infant developed typical respiratory distress syndrome despite the normal total lecithin concentration of amniotic fluid at birth. The fatty acid analysis, however, revealed that the surfactant lecithin concentration was extremely low, showing a great discrepancy between total lecithin and surfactant lecithin concentrations. Thus the estimation of disaturated and/or dipalmitoyl lecithin in the amniotic fluid seems to be the most precise sign of a potential risk of respiratory distress syndrome.

Amniotic Fluid↗
PubMed1975

Mechanism of secretion of biliary lipids. I. Role of bile canalicular and microsomal membranes in the synthesis and transport of biliary lecithin and cholesterol.

The role of bile canalicular and microsomal membranes in the synthesis and transport of biliary lipids was investigated by using the isolated perfused rat liver model. Labeled lecithin precursors ((3H)-palmitic acid, (14C)linoleic acid, (3H)choline, and 32PO4) and a cholesterol precursor ((3H)mevalonic acid) were administered with and without sodium taurocholate. The incorporation pattern of these labeled precursors into linoleyl and arachidonyl lecithins and cholesterol fractions of microsomes, bile canaliculi, and bile were examined at 30-min intervals up to 90 min. Marker enzymes and electron microscopy indicated that isolated subfractions of plasma membranes were enriched with bile canaliculi (less than 10 percent microsomal contamination). Taurocholate significantly stimulated the incorporation of 32PO4, (3H)choline, (3H)palmitic acid, and (14C)linoleic acid into linoleyl and arachidonyl lecithin with parallel incorporation curves for microsomal and bile canalicular membranes throughout the 90-min study period. During the 30-60-min period, however, these same lecithin fractions in bile significantly exceeded the specific activity of the membrane lecithins. The enzyme CDP-choline diglyceride transferase was virtually absent from canaliculi relative to microsomes, indicating that canaliculi lack the capacity for de novo lecithin synthesis. Incorporation of (3H)mevalonic acid into membranous and biliary cholesterol followed a pattern similar to that for lecithin. These data provide evidence that (a) biliary lecithin and cholesterol are derived from a microsomal subpool regulated by the flux of enterohepatic bile acids, (b) the role of the bile canalicular membranes with respect to biliary lipids is primarily transport rather than synthesis, and (c) lecithin and cholesterol are transported together from microsomes to bile. The findings are consistent with the existence of a cytoplasmic lipid complex within the hepatocyte which is actively involved in the intermembrane transport of biliary lipid.

Animals↗
PubMed1993

Lecithin in swine diets: I. Weanling pigs.

One digestibility experiment (Exp. 1) and two growth experiments (Exp. 2 and 3) were conducted to evaluate the use of lecithin as an emulsifier of soy oil and(or) an energy source in a two-phase starter diet program. Phase 1 consisted of d 0 to 14 postweaning, and Phase 2 consisted of d 14 to 35 postweaning. Diets were based on corn, soybean meal, and 20% dried whey and contained a constant ME:lysine level. In Exp. 1 and 2, two levels of lecithin (0 and 2%) at two levels of soy oil (0 and 6%) were investigated. In both experiments, there was no interaction between lecithin and soy oil for any traits measured. In Exp. 1, the apparent digestibility of fat increased significantly with increased fat level in the diets. Addition of lecithin to diets improved (P < .05) nitrogen retention, and the addition of soy oil significantly improved apparent digestibility of DM, GE, fat, and CP. In Exp. 2, there was no significant effect of lecithin or soy oil on ADG. In Phase 2 and overall, the inclusion of lecithin and soy oil to diets significantly increased gain/feed but did not significantly improve gain/ME intake. In Exp. 3, pigs were fed diets containing 0, 1, 2, or 3% lecithin. The addition of lecithin to diets did not affect ADG, ADFI, gain/feed, or gain/ME intake during Phases 1, 2, or overall. These results fail to demonstrate that the addition of lecithin to diets for young pigs improves utilization of soy oil or growth performance.

Animal Feed↗
PubMed1999

A fluorescence energy transfer study of lecithin-cholesterol vesicles in the presence of phospholipase C.

We demonstrate Förster resonance energy transfer from dehydroergosterol to dansylated lecithin in lecithin-cholesterol vesicles and characterize the vesicles in the presence of the pro-nucleating enzyme, phospholipase C (PLC). Exposure to phospholipase C causes a temporary decrease in the dehydroergosterol to dansyl fluorescence ratio followed by an increase to and above the initial value. The temporary decrease in the fluorescence ratio results from an increase in the dansylated lecithin intensity that coincides with a dansyl blue shift. The extent of the blue shift correlates with the level of diacylglycerol generated in situ by PLC, suggesting an increased association between dansylated lecithin and cholesterol as membrane fluidity increases and membrane polarity decreases. The subsequent increase in the fluorescence ratio results from both an increase in the dehydroergsterol intensity and a concomitant decrease in the dansylated lecithin intensity of equal magnitude. This signifies a reduction in energy transfer from dehydroergosterol to dansylated lecithin and indicates an increased separation between the two fluorophores. The increase in the fluorescence ratio persists beyond the time scales for vesicle aggregation and fusion, as measured by turbidity, and precedes the onset of macroscopic cholesterol crystals observed with an optical microscope. Thus, the increased separation between dehydroergosterol and dansylated lecithin is consistent with a mechanism of cholesterol nucleation from the vesicles. Moreover, the onset and rate of increase in the fluorescence ratio correlate with the cholesterol:lecithin mole ratio of the vesicles. Fluorescence energy transfer from dehydroergosterol to dansylated lecithin therefore shows potential as a methodology for measuring cholesterol nucleation in model bile.

Cholesterol↗
PubMedDate not supplied

[Lecithin essay in the diet of young Penaeus vannamei (Crustacea: Decapoda)].

The effect of different lecithin sources and presentations on growth, food conversion ratio and survival of P. vannamei (290 mg +/- 0.02) was studied. The bioassay was designed in order to compare different dietary levels and different quality of lecithin. Squid lecithin, crude soybean (7%), deoiled soybean lecithin (3.48%) in combination with fish oil or squid neutral lipids, in a partially dilapidate formula. The isoenergetic diets were fed ad libitum to four replicate groups (tanks) of 15 shrimps each (5 x 4 x 15), during 28 days. The result of the bioassay with the partially dilapidate formulas was; the best growth rate (191%) and FCR (1.69 +/- 0.041) were obtained with the diet containing 7% of soybean crude lecithin as the unique lipid source. Followed by the diet countering 3.94% deoiled lecithin and 2.42% Menhaden oil (172% and 2.03 +/- 0.054 respectively). As expected, the worst results were obtained without the dietary lecithin 121% and 2.42 +/- 0.129). Crude soybean lecithin alone covered the phospholipid and neutral lipids requirements as well as the combination of deoiled soybean lecithin with fish or squid oil.

Animal Feed↗
PubMed1969

Molecular species of lecithins from erythrocytes and plasma of man.

The lecithins of the plasma and erythrocytes of man were isolated by thin-layer chromatography, and the major molecular species were identified and quantitatively estimated by combined thin-layer and gas-liquid chromatography and specific enzymic hydrolyses. Using these techniques we could identify over 60 molecular species, accounting for some 98% of the total lecithin, in both plasma and cells, but only about 30 of them occurred in concentrations over 1%. The molecular species of lecithins in the cells and plasma were qualitatively similar; quantitatively, large differences were noted among and within the various classes of unsaturation. In the same blood, the erythrocyte lecithins contained 8-20 times as high a percentage of saturated lecithins and nearly twice as high a percentage of monounsaturated lecithins as did plasma lecithins. The differences in the relative amounts of a particular molecular species within a class of unsaturation were, however, most pronounced among the polyunsaturated lecithins. These results suggest that plasma and red cells possess distinct lecithin populations and that complete equilibration of the intact molecules between the two media is unlikely.

Acetates↗
PubMed1966

In vivo studies on pathways for the biosynthesis of lecithin in the rat.

The in vivo biosynthesis of lecithin in rats has been studied with the precursors choline-1,2-(14)C, ethanolamine-1,2-(14)C and methionine-CH(3)-(14)C or -CH(3)-(3)H. Lecithin synthesis from choline is rapid in all organs. No sex difference was observed in this pathway. The biosynthesis of lecithin by methylation of phosphatidyl ethanolamine is of quantitative significance in the liver, but not in extrahepatic tissues. More lecithin is synthesized by this pathway in female rats. In liver the lecithin synthesized via both pathways enters a common pool which is in rapid equilibrium with lecithin of blood plasma. A sex difference in the utilization of radioactive ethanolamine for the formation of phosphatidyl ethanolamine was observed (greater utilization in the female). Incorporation of ethanolamine into phospholipids of extrahepatic tissues was slow in both sexes. With labeled methionine as precursor the liver cytidine diphosphate (CDP) choline had a specific activity identical with that of liver lecithin after 20 min, while the specific activity of phosphoryl choline remained low. With labeled choline as precursor the phosphoryl choline reached a specific activity 50 times that of lecithin after 20 min, while the specific activity of CDP choline was only four times that of lecithin. These findings indicate that the reaction: CDP choline + diglyceride right harpoon over left harpoon phosphatidyl choline + CMP is freely reversible in vivo.

Amines↗
PubMed1956

Use of synthetic, crystalline, L-alpha-dimyristoyl lecithin in cardiolipin antigens.

Experiments were carried out by the authors to determine whether synthetic, crystalline, L-alpha-dimyristoyl lecithin could replace natural purified lecithins in the preparation of cardiolipin antigens. These experiments were designed specifically to find out whether it was possible to obtain the same serological reactions, qualitatively and quantitatively, with the test antigen as with a reference antigen containing natural lecithin, and whether the test antigen had the same keeping qualities as the reference antigen.The tests used were the quantitative complement-fixation test as modified by Mørch in 1933, and the VDRL slide flocculation test.The results showed that synthetic, crystalline, L-alpha-dimyristoyl lecithin could replace natural lecithin in the preparation of cardiolipin antigens, but that the antigens prepared with the synthetic lecithin were significantly less sensitive than those prepared with an equimolar amount of natural lecithin. The authors consider that further investigation is required before the use of synthetic lecithin is finally adopted.

Cardiolipins↗
PubMed1992

Polyunsaturated lecithin prevents acetaldehyde-mediated hepatic collagen accumulation by stimulating collagenase activity in cultured lipocytes.

We recently found that polyunsaturated lecithin prevents ethanol from causing cirrhosis in the baboon. Because transformation of lipocytes to transitional cells plays a key role in hepatic fibrogenesis in vivo, and because this process in alcohol-fed baboons was found to be attenuated by polyunsaturated lecithin, we focused on lipocytes to study the mechanism of the protective effect. Rat lipocytes cultured on plastic undergo spontaneous activation, accompanied by expression of alpha-smooth muscle actin isoform and production of substantial amounts of type I collagen. The latter was further increased on incubation with acetaldehyde. This in vitro model was used here to study how acetaldehyde-mediated collagen production and accumulation can be turned off. Addition of polyunsaturated lecithin (10 mumols/L) was found to prevent the acetaldehyde-induced increase in collagen accumulation by 83% (p less than 0.001). By contrast, a saturated phospholipid (10 mumols/L dilauroyl phosphatidylcholine), a monounsaturated one (10 mumols/L linoleoyl-palmitoyl phosphatidylcholine) or linoleic acid (20 mumols/L bound to albumin) had no such effect. Incorporation of [3H]proline into collagen and the expression of alpha-1 (I) procollagen mRNA were increased by acetaldehyde; the latter was not significantly affected by polyunsaturated lecithin. Polyunsaturated lecithin increased lipocyte collagenase activity by 100% (p less than 0.001), whereas dilauroyl phosphatidylcholine, linoleoyl-palmitoyl phosphatidylcholine and linoleic acid had no such action. We concluded that (a) polyunsaturated lecithin selectively prevents the acetaldehyde-induced increase in collagen accumulation in lipocyte cultures, whereas other phospholipids or linoleate have no such effect; and (b) polyunsaturated lecithin does not modify the acetaldehyde-mediated increase in alpha-1 (I) procollagen mRNA, but it increases collagenase activity, suggesting that the protective effect exerted by polyunsaturated lecithin against alcohol induced fibrosis in vivo is due at least in part to stimulation of collagenase activity, which may prevent excess collagen accumulation by offsetting increased collagen production.

Acetaldehyde↗
PubMed1998

Lecithin protects against plasma membrane disruption by bile salts.

INTRODUCTION: Detergent disruption of epithelial plasma membranes by bile salts may contribute to pathogenesis of cholestasis and gastroesophageal reflux disease. Bile, despite containing high concentrations of bile salts, normally is not toxic to biliary or intestinal epithelia. We hypothesize that lecithin in bile may protect cell membranes from disruption by bile salts. METHODS: We studied the interactions of taurine conjugates of ursodeoxycholate (TUDCA), cholate (TCA), chenodeoxycholate (TCDCA), and deoxycholate (TDCA) with erythrocyte plasma membranes with or without large unilamellar egg lecithin vesicles for various times at 23 degreesC. Release of hemoglobin was quantified spectrophotometrically. The concentration of bile salt monomers and simple micelles in the intermixed micellar aqueous phase (IMMC) was determined by centrifugal ultrafiltration. RESULTS: The degree of hemolysis depended on the hydrophobicity of the bile salts and was progressive over time. Addition of lecithin reduced the hemolytic effects of 20 mM TCA or 2 mM TDCA in a concentration-dependent manner at both 30 min and 4 h. Increasing the concentration of lecithin progressively reduced the IMMC of TDCA. Hemolysis following addition of lecithin to 2 mM TDCA was comparable to hemolysis produced by lecithin-free TDCA solutions when diluted to similar IMMC values. CONCLUSION: We conclude that lecithin reduces plasma membrane disruption by hydrophobic bile salts. This protection may be attributable to association of bile salts with vesicles and mixed micelles, reducing the concentration of bile salt monomers and simple micelles available to interact with cell membranes. Lecithin may play a key role in preventing bile salt injury of biliary and gastrointestinal epithelia.

Bile Acids and Salts↗
PubMed1976

Lecithin inhibits fatty acid and bile salt absorption from rat small intestine in vivo.

During digestion of a fatty meal, long chain free fatty acids (FFA) and lecithin are among the lipids solubilized in intestinal contents as mixed micelles with bile salts. We hypothesized that if lecithin were not hydrolyzed, the mixed micelles would be abnormal, and absorption of FFA and bile salts would be depressed. To test this hypothesis, isolated segments of rat small intestine were infused in vivo with micellar solutions of 2 mMolar linoleic acid and 10 mMolar taurocholate to which was added 3 mMolar 1-palmitoyl, 2-oleoyl lecithin (a common lecithin in bile and food), or 1-palmitoyl lysolecithin (the hydrolytic product of lecithin). Absorption of FFA and bile salt was measured under steady state conditions using a single-pass technique. Lecithin depressed the rate of FFA absorption by 40% (p less than 0.025) in jejunal and ileal segments whereas lysolecithin was associated with normal rates of FFA absorption. Lecithin also reduced taurocholate absorption from the ileum by 30% (p less than 0.05). These data support the idea that lecithin may depress FFA and bile salt absorption from the small intestine in pancreatic insufficiency.

Animals↗
PubMed1988

Influence of dietary soybean and egg lecithins on lipid responses in cholesterol-fed guinea pigs.

The comparative influence on plasma and tissue lipids of dietary soybean and egg lecithins, which have contrasting fatty acid compositions, was studied in the hypercholesterolemic guinea pig. The polyunsaturated to saturated fatty acid (P/S) ratios of the soybean and egg lecithins were 3.4 and 0.38, respectively. Hypercholesterolemia was induced by feeding guinea pigs a purified diet that contained 15% lard enriched with 0.5% cholesterol. Subsequently, guinea pigs were fed for six wk the same diet supplemented with either soybean or egg lecithin as 7.5% of the diet. A control group continued to be fed the lecithin-free diet. Parameters measured included body weight and relative liver weight; in plasma, total cholesterol, high density lipoprotein cholesterol (HDLC), phospholipid, and nonesterified cholesterol; in liver, total fat, cholesterol, and the specific activity of the catabolic enzyme cholesterol 7 alpha-hydroxylase; (EC 1.14.13.17); and in the aorta, cholesterol. Among the most noteworthy observations were the 49% decrease in total plasma cholesterol of the soybean lecithin group without decreasing HDLC and the 177% increase in HDLC of the egg lecithin group without a significant increase in total cholesterol compared with those values in the control group. These data suggest that dietary lecithin is particularly effective in increasing the HDLC/total cholesterol ratio in plasma. However, the absolute concentrations of those plasma lipids seem to depend upon the fatty acid composition of the lecithin.

Animals↗
PubMed2004

Partial characterization of cytoprotective mechanisms of lecithin against bile salt-induced bile duct damage.

BACKGROUND: We recently demonstrated that cyclosporine A causes a disproportionate reduction of biliary lipid secretion, and this is inhibited by hydrophilic bile salts through the enhancing of biliary lecithin secretion. In the present study, the underlying mechanism of such a cytoprotective action of hydrophilic bile salts was determined with attention to the possible role of lecithin. METHODS: Immortalized mouse cholangiocytes were cultured for 4 h with taurine conjugates of a hydrophobic bile salt (cholate [TC]), and hydrophilic bile salts (ursodeoxycholate [TUDC], betamuricholate [TbetaMC], and alphamuricholate [TalphaMC]), at 200 microM, in the presence or absence of lecithin (5, 10, 25, 50, 100, or 200 microM), followed by flow cytometric detection of apoptosis, using Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining. Cholangiocyte bile salt transporter mRNAs (apical sodium-dependent bile-salt transporter [Asbt] and multidrug resistance protein 3 [Mrp3]) were determined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Apoptosis was induced by all of the bile salts (TC > TUDC, TbetaMC, and TalphaMC). Interestingly, bile salt-induced apoptosis was inhibited by lecithin in a concentration-dependent manner. Further, RT-PCR showed that the expressions of Asbt and Mrp3 mRNAs were enhanced by all the bile salts, whereas lecithin reduced Asbt expression, but enhanced Mrp3 expression. CONCLUSIONS: These findings indicate that bile salts cause bile-duct cell damage through Asbt-mediated uptake, but that biliary lecithin physiologically inhibits such damage by reducing the expression of this transporter. In addition, the induction of Mrp3 expression by lecithin may play a role in inhibiting the accumulation of bile. Thus, the modulation of lecithin secretion into bile may be another important target for the treatment of biliary disorders.

Animals↗
PubMed1978

Determination of disaturated lecithin in rhesus monkey amniotic fluid as an index of fetal lung maturity.

Although increased concentrations of total lecithin in amniotic fluid allow prenatal assessment of fetal lung maturation, it has become clear that routine use of the L/S index may lead to a substantial number of inaccurate predictions. Since disaturated lecithin (DL) is a more specific marker of pulmonary surfactant than total lecithin, we developed a convenient method for measuring this phospholipid in amniotic fluid, and then evaluated its level in pregnant rhesus monkeys of 120 to 163 days of gestation. The method involves osmic acid destruction of unsaturated lipids, chromatographic isolation of disaturated lecithin, and quantitation by phosphorus assay. It can be performed in approximately 5 hours on 4 ml. of amniotic fluid and yield 67 +/- 3 per cent average recovery of added 14C-dipalmitolyl lecithin. The results of analyzing 36 rhesus amniotic fluid specimens showed the disaturated lecithin and the disaturated lecithin/sphingomyelin ratio (DL/S) increase sharply after 150 days of gestation, consistent with the pattern of lung maturation in this species. We conclude that disaturated lecithin can be readily quantitated in primate amniotic fluid and that its concentration, the DL/S ratio, and percentage of disaturated lecithin are potentially useful indices of fetal lung maturity for the clinical laboratory.

Amniotic Fluid↗
PubMed1980

Influence of lecithin liposomes on chlorophyllase-catalyzed chlorophyll hydrolysis: comparison of intramembraneous and solubilized Phaeodactylum chlorophyllase.

1.Chlorophyllase-catalyzed chlorophyll hydrolysis is greatly enhanced by the addition of divalent cations (Mg2+) combined with a reducing agent (dithiothreitol, ascorbate). A similar effect is obtained by the addition of lecithin. In the presence of lecithin, dithiothreitol has only slight or no influence on chlorophyll hydrolysis. Mg2+ eliminates the activating effect of lecithin. 2. In the absence of Mg2+ + dithiothreitol or of lecithin, Triton X-100 has a slight activating effect on chlorophyllase-catalyzed chlorophyll hydrolysis, but only at low concentrations (0.01--0.02%). In the presence of Mg2+ and dithiothreitol or of lecithin, Triton X-100 (greater than or equal to 0.02%) inhibits this reaction. 3. Whereas chlorophyllase combines with chlorophyll, no combination of chlorophyllase and lecithin could be detected. 4. Solubilized chlorophyllase is stabilized by its substrate, chlorophyll. Enzyme stabilization is eliminated by lecithin, whereas in the absence of chlorophyll, denaturation is somewhat increased by dithiothreitol. 5. No clear difference was found between the actions of intramembraneous and solubilized chlorophyllase. The results suggest that chlorophyllase is situated within membranes in such a way that the active group protrudes into the aqueous medium surrounding the membrane. 6. A hypothesis explaining the activating effects which Mg2+ combined with a reducing agent and lecithin have upon chlorophyllase-catalyzed chlorophyll hydrolysis is presented.

Chlorophyll↗
PubMed1983

Interspecies activation of lecithin-cholesterol acyltransferase by apolipoprotein A-I isolated from the plasma of humans, horses, sheep, goats and rabbits.

The abilities of apolipoprotein A-I species isolated from humans, horses, sheep, goats and rabbits to activate purified human lecithin-cholesterol acyltransferase and the enzyme from homologous plasmas and plasma of other mammalian species were compared. Each purified apolipoprotein A-I species was individually incorporated into phosphatidylcholine/cholesterol vesicles by the cholate dialysis method to form proteoliposome common substrates (apolipoprotein A-I/phosphatidylcholine/cholesterol molar ratio of 1:250:12.5) for the enzyme activity assay. All apolipoprotein A-I species tested had the ability, but with different effectiveness, to activate plasma lecithin-cholesterol acyltransferase from their own and other animal species and from purified human lecithin-cholesterol acyltransferase. Horse apolipoprotein A-I was nearly as effective as human apolipoprotein A-I, whereas apolipoproteins A-I from goats, sheep or rabbits were, in descending order, slightly less effective than either horse or human apolipoprotein A-I in activating human plasma lecithin-cholesterol acyltransferase. A similar trend in ability to activate purified human lecithin-cholesterol acyltransferase by these apolipoprotein A-I species was seen, but apolipoprotein A-I from sheep, goats and rabbits was only about 55-65% as effective as human apolipoprotein A-I. In general, apolipoprotein A-I from the same animal species as the lecithin-cholesterol acyltransferase enzyme was a better activator of the enzyme than was apolipoprotein A-I from another animal species. Comparison of lecithin-cholesterol acyltransferase activities of each plasma paired with its own apolipoprotein A-I, which reflects the level of the enzyme in the plasma, revealed descending levels of the enzyme's activity (nmol/h per ml) as follows: humans (98.9 +/- 10.3), horses (90.7 +/- 10.6), sheep (69.9 +/- 9.7), goats (64.9 +/- 9.2) and rabbits (52.0 +/- 6.2). Studies with DEAD-Sepharose columns, gel electrophoresis, and proteoliposome substrates demonstrated that apolipoprotein A-I from these mammalian species are similar in molecular charge and weight and are functionally similar in lecithin-cholesterol acyltransferase activation.

Animals↗