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PubMed1993

Lipid and fatty acid composition of brain tissue from adrenoleukodystrophy patients.

White matter and active plaque tissue from adrenoleukodystrophy (ALD) patients were analysed for lipid class and fatty acid compositions and the results compared with white matter from normal brain. ALD white matter was characterised by increased levels of cholesteryl esters and decreased levels of phosphatidylethanolamine, including phosphatidylethanolamine plasmalogen, in comparison with normal brain white matter. In addition to even higher levels of cholesteryl esters, ALD plaque tissue had reduced levels of cerebrosides as well as phosphatidylethanolamines. The loss of phosphatidylethanolamine plasmalogen is indicative of early demyelination. Total lipid from ALD white matter and ALD plaque tissue contained nearly five times and seven times, respectively, more 26:0 than total lipid from normal brain white matter. The 26:0 in ALD white matter was elevated in all lipid classes except phosphatidylinositol, but was located mainly in cerebrosides, phosphatidylcholine, sphingomyelin, and sulfatides. Most of the 26:0 in ALD plaque tissue was present in cholesteryl esters, followed by phosphatidylcholine and sphingomyelin, with reduced amounts in cerebrosides as compared with ALD white matter. The results are consistent with an initial accumulation of very-long-chain fatty acids in ALD white matter, primarily in sphingolipids and phosphatidylcholine, and subsequent accumulation of very-long-chain fatty acids in cholesteryl esters during demyelination. In addition, it was notable that the sphingolipids, especially sphingomyelin in ALD brain, had decreased levels of 24:1 and increased levels of 18:0, as well as increased levels of very-long-chain fatty acids. The extent to which the data shed light on mechanisms of demyelination in ALD is discussed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenoleukodystrophy↗

PubMed2004

Changes in phospholipid content and myocardial calcium-independent phospholipase A2 activity during chronic anthracycline administration.

Despite numerous investigations, the causes underlying anthracycline cardiomyopathy are yet to be established. We have recently reported that acute treatment with anthracyclines inhibits membrane-associated calcium-independent phospholipase A(2) (iPLA(2)) activity both in vitro and in vivo. This study presents data that iPLA(2) activity is also suppressed during chronic drug administration. Adult Sprague-Dawley rats were given weekly 1 mg/kg i.v. injections of doxorubicin for a total of 8 weeks. One week after the last injection, the animals were sacrificed, and heart tissue was assessed for phospholipid content and iPLA(2) activity. Membrane-associated iPLA(2) activity in the myocardium of doxorubicin-treated animals was 40% lower than that in control hearts. In addition, doxorubicin treatment resulted in significant alterations in the distribution of fatty acyl moieties esterified to the sn-2 position of choline glycerophospholipids. The ethanolamine species remained unaffected. Elevation in the amount of arachidonate and linoleate esterified to the sn-2 position of choline plasmalogens was consistent with the hypothesis that iPLA(2) displays selectivity for plasmalogen phospholipids; therefore, enzyme inhibition may affect hydrolysis of these phospholipid subclasses. Notably, the changes in phospholipid content occurred at a low cumulative dose of 8 mg/kg at which appearance of structural lesions was minimal. Therefore, these alterations seem to be both specific and early signs of cardiomyocyte pathology. The results support our hypothesis that myocardial iPLA(2) inhibition may be one of the steps that leads to the functional and structural changes associated with chronic anthracycline treatment.

Animals↗

PubMed1982

Isolation and characterization of new strains of cholesterol-reducing bacteria from baboons.

We isolated and characterized nine new strains of cholesterol-reducing bacteria from feces and intestinal contents of baboons. Cholesterol-brain agar was used for the primary isolation, and subsequent biochemical tests were done in a lecithin-cholesterol broth containing plasmenylethanolamine and various substrates. All strains had similar colony and cell morphology, hydrolyzed the beta-glucosides esculin and amygdalin, metabolized pyruvate, and produced acetate and acetoin. Unlike previously reported strains, the nine new strains did not require cholesterol and an alkenyl ether lipid (e.g., plasmalogen) for growth; however, only two strains reduced cholesterol in the absence of the plasmalogen. These two strains also produced succinate as an end product. Carbohydrate fermentation was variable; some strains produced weak acid (pH 5.5 to 6.0) from only a few carbohydrates, whereas other strains produced strong acid reactions (pH less than or equal to 5.5) from a wide variety of carbohydrates.

Animals↗

PubMed1980

Isolation and characterization of outer and inner membranes of Selenomonas ruminantium: lipid compositions.

The isolation procedure and characterization of the outer and inner membranes from Selenomonas ruminatium cells, a strictly anaerobic bacterium, are described. The metabolic fate of [14C]decanoate incorporated into the outer and inner membranes was examined. The percent distribution of radioactivities in the outer and inner membranes was about 40 and 50% of the total incorporated activity, respectively. Approximately 47% of the radioactivity incorporated into the outer membrane was recovered in the phospholipid fraction, and the remaining radioactivity was found in both aqueous and phenol layers when the outer membrane was treated with phenol-water. In contrast to [14C]decanoate, the percent distribution of [3H]glycerol in the outer and inner membranes was about 25 and 70% of the total incorporated activity, respectively. Most of the assimilated 3H was located in the phospholipid fraction of both membranes. However, no significant label was detected in either the protein or cell wall fraction. The following observations were made concerning lipid compositions in the outer and inner membranes by chemical and isotopic analyses. (i) The outer and inner membranes contained no detectable phosphatidyl glycerol or cardiolipin. (ii) A prominent radioactive compound, designated band III lipid, was found mainly in the outer membrane as a major radioactive spot when cells were grown with [14C]decanoate. This lipid contained phosphorus, 2-keto-3-deoxyoctulosonic acid and 3-OH fatty acid but no detectable glycerol. This lipid was identified tentatively to be 2-keto-3-deoxyoctulosonic acid-lipid A. (iii) Although the ubiquity of phosphatidyl ethanolamine plasmalogen in both outer and inner membranes was confirmed, the occurrence of the molecular species of phosphatidyl ethanolamine plasmalogen was quite different in the outer and inner membranes.

Aldehydes↗

PubMed1981

Phospholipid biosynthesis in some anaerobic bacteria.

We have identified and characterized enzymes of phospholipid synthesis in two plasmalogen-rich anaerobes. Megasphaera elsdenii and Veillonella parvula, and one anaerobe lacking plasmalogens. Desulfovibrio vulgaris. All three species contained phosphatidate cytidylyltransferase and phosphatidylserine synthase. Phosphatidylglycerophosphate synthesis was detected only D. vulgaris extracts. Phosphatidylserine (diacyl form) was the major product of the phosphatidylserine synthase assay with particles from M. elsdenii or V. parvula. The amounts of phosphatidylethanolamine formed were very low. Only D. vulgaris particles had an active phosphatidylserine decarboxylase.

CDPdiacylglycerol-Serine O-Phosphatidyltransferase↗

PubMed1976

Comparative study of the lipid composition of rabbit and lobster sarcoplasmic reticulum.

Sarcoplasmic reticulum (SR) membranes isolated from rabbit and lobster muscles have similar phospholipid classes, but they differ in plasmalogen content. The plasmalogenic species are mostly distributed among phosphatidylethanolamines (PE's) and make up about 62% of the total in rabbit SR and about 46% in lobster membranes. Lobster SR phospholipids contain large amounts of polyunsaturated fatty acids which are present in low amounts in rabbit membranes. The total unsaturated fatty acids of phosphatidylcholines (PC's) represent about 53% and 73% of the total fatty chains for rabbit and lobster SR, respectively. The values found for PE's were about 56% and 64%, respectively. Furthermore, lobster membranes contain significant amounts of PC and PE molecular species with unsaturated fatty acids in positions 1 and 2, whereas rabbit SR contain low amounts.

Adenosine Triphosphatases↗

PubMed2005

Activation of MAPKs in thrombin-stimulated ventricular myocytes is dependent on Ca2+-independent PLA2.

Thrombin stimulation of isolated rabbit ventricular myocytes activates a membrane-associated, Ca(2+)-independent PLA(2) (iPLA(2)) that selectively hydrolyzes plasmalogen phospholipids and results in increased production of arachidonic acid and lysoplasmenylcholine. To determine whether MAPK regulates myocardial iPLA(2) activity, we isolated ventricular myocytes from rabbit heart by collagenase digestion and pretreated them with MAPK inhibitors before stimulating them with thrombin. Pretreatment with PD-98059 to inhibit p42/44 MAPK or SB-203580 to inhibit p38 MAPK had no significant effect on thrombin-stimulated, membrane-associated iPLA(2) activity. Thrombin stimulation resulted in significant increases in both p42/44 and p38 MAPK activity after 2 min. Pretreatment with the iPLA(2)-selective inhibitor bromoenol lactone completely inhibited thrombin-stimulated MAPK activity, suggesting that activation of MAPKs was dependent on iPLA(2) activation. Ventricular myocyte MAPK activity was increased by incubation of the myocytes with lysoplasmenylcholine, a metabolite produced by iPLA(2)-catalyzed membrane plasmalogen phospholipid hydrolysis. Altogether, these data suggest that activation of MAPKs occurs downstream of and is dependent on iPLA(2) activation in thrombin-stimulated rabbit ventricular myocytes.

Animals↗

PubMed2005

Neutrophil-mediated accumulation of 2-ClHDA during myocardial infarction: 2-ClHDA-mediated myocardial injury.

The pathophysiological sequelae of myocardial infarction include neutrophil infiltration into the infarct zone that contributes to additional damage to viable tissue and removal of cellular debris from necrosed tissue. Reactive chlorinating species produced by myeloperoxidase amplify the oxidant capacity of activated neutrophils. Plasmalogens are a major phospholipid subclass of both endothelial cells and cardiac myocytes. Recent studies have shown that plasmalogens are targeted by neutrophil-derived reactive chlorinating species that lead to the production of alpha-chloro fatty aldehydes. Results herein demonstrate that the alpha-chloro fatty aldehyde 2-chlorohexadecanal (2-ClHDA) accumulates in rat hearts subjected to left anterior descending coronary artery occlusion. Myocardia from rats subjected to surgical infarction had increased 2-ClHDA and neutrophil infiltration levels compared with myocardia from rats subjected to sham surgery. Additionally, infarcted myocardia from rats rendered neutropenic by treatments with an anti-neutrophil antibody had diminished 2-ClHDA and neutrophil infiltration levels compared with infarcted myocardia from normopenic rats; 2-ClHDA was shown to elicit myocardial damage as determined by lactate dehydrogenase release in isolated perfused rat hearts. Additionally, 2-ClHDA treatment of hearts resulted in decreased heart rate and ventricular performance. Taken together, the present results demonstrate a novel neutrophil-dependent myeloperoxidase-based mechanism that results in 2-ClHDA production in response to regional myocardial infarction that may also contribute to cardiac dysfunction.

Aldehydes↗

PubMed1978

Pelizaeus-Merzbacher disease: biochemical analysis of isolated myelin (electron-microscopy; protein, lipid and unsubstituted fatty acids analysis).

Analysis of myelin from a leukodystrophic brain was performed (Pelizaeus-Merzbacher disease, classical type). Myelin recovery was 7% of normal, when isolated by ultracentrifugation. Electron microscopy showed a great amount of loose lamellae, with less thick sheaths and periodicity close to normal. This myelin contains fewer lipids than normal, sphingolipids and plasmalogens being reduced. FAtty acids from phospholipids are essentially normal, however enols from plasmalogens are largely reduced. Purified sphingolipids (cerebrosides, sulfatides and sphingomyelin) present a considerable diminution in very long chain fatty acids; the ratio of very long chain fatty acids (over C18) on shorter chains is 1% of the normal value for saturated fatty acids and 2% for the monounsaturated homologues. Protein analysis showed that basic protein and proteolipids were reduced, Wolfgram proteins being relatively increased.

Brain Chemistry↗

PubMed1995

Distribution of membrane phospholipids in the rabbit uvea.

BACKGROUND AND AIMS: Since the uveal tract becomes involved in inflammatory disorders, which are known to affect lipid metabolism, we studied normal membrane phospholipids (PLs) in order to (1) determine baseline PL profiles of the iris, ciliary body, and choroid, and (2) compare and contrast PL profiles of the uveal tissues. METHODS: Iris, ciliary body and choroid tissues were isolated from rabbit eyes (n = 30) and extracted with chloroform-methanol using a modified Folch procedure. Quantitative tissue PL profiles were obtained using 31P nuclear magnetic resonance. RESULTS: Fourteen PLs were detected and quantitated in all three uveal tissues among which was one unidentified PL at -0.17 ppm. The five major PLs in the iris, ciliary body and choroid, respectively, have the following PL composition (mole percent of total phosphorus): ethanolamine plasmalogen 14.58, 15.07, 16.52; phosphatidylethanolamine 13.10, 12.40, 9.23; phosphatidylserine 11.24, 10.27, 12.13; sphingomyelin (SM) 11.10, 11.97, 18.21; and phosphatidylcholine (PC) 36.61, 36.70, 29.88. Additionally, lysophosphatidic acid, phosphatidic acid, lysophosphatidylcholine, phosphatidylinositol, and PC plasmalogen or alkacyl PC were detected in all tissues. Sphingosylphosphorylcholine also was detected in the ciliary body and choroid. Lysophosphatidylethanolamine was detected in the choroid. In addition, 42 PL metabolic indexes were calculated from these data, which permitted pathway-specific lipid analyses. CONCLUSION: This study establishes baseline PL profiles of the uveal tract tissues and will permit comparisons with tissues from eyes with inflammatory disorders. The PL concentrations in conjunction with the indexes demonstrate that overall the choroid has membranes that are less permeable to ion translocation than either the iris or the ciliary body, although there are compensatory concentration changes between the SM and PC components among these three tissues.

Animals↗

PubMed1992

Lysoplasmenylethanolamine accumulation in ischemic/reperfused isolated fatty acid-perfused hearts.

Lysophospholipid accumulation has been implicated in the pathogenesis of irreversible injury during myocardial ischemia and reperfusion. Plasmalogens (phospholipids with a vinyl-ether bond in the sn-1 position) account for more than 50% of total myocardial sarcolemmal and sarcoplasmic reticulum phospholipids. Accumulation of plasmalogen choline and ethanolamine lysophospholipids (lysoplasmenylcholine and lysoplasmenylethanolamine) or the effects of exogenous fatty acids on lysoplasmalogen accumulation during ischemia and reperfusion have not been examined. Isolated working rat hearts perfused with buffer containing either 11 mM glucose or 11 mM glucose plus 1.2 mM palmitate were subjected to aerobic, ischemic, or ischemia/reperfusion protocols. Levels of lysoplasmenylcholine and lysoplasmenylethanolamine were quantified using a two-stage high-performance liquid chromatographic technique. In hearts perfused with glucose alone, no significant differences in levels of lysoplasmenylcholine or lysoplasmenylethanolamine were seen during ischemia or reperfusion. In fatty acid-perfused hearts, however, significant accumulation of lysoplasmenylethanolamine occurred during reperfusion but not during ischemia (723 +/- 112, 734 +/- 83, and 1,394 +/- 193 nmol/g dry wt for aerobic, ischemic, and ischemic/reperfused hearts, respectively; p less than 0.05 for ischemic/reperfused hearts versus aerobic or ischemic hearts). Lysoplasmenylcholine levels after ischemia and reperfusion did not differ significantly from aerobic values, regardless of whether fatty acids were present or absent from the perfusate. Aerobic and ischemic/reperfused rabbit hearts, in the presence of fatty acid, showed a similar profile in their lysoplasmalogen content. We conclude that differential lysoplasmenylethanolamine accumulation occurs during myocardial reperfusion when exogenous fatty acid concentrations are high. This may reflect the selective action of fatty acid intermediates on the metabolism of lysoplasmenylethanolamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Two siblings with phenotypes mimicking peroxisomal disorders but with discordant biochemical findings.

The authors present a report on two sibling with a nearly identical phenotype mimicking peroxisomal disorder but with totally discordant biochemical findings. In an attempt to confirm the diagnosis of a peroxisomal disorder, plasma levels of very long chain fatty acids (VLCFA) and phytanic acid were determined. In addition, fibroblasts profile of VLCFA and plasmalogen levels were evaluated for Case 2. Pathomorphological examinations represented by lymph node and kidney biopsies as well as postmortem examinations of liver, adrenals and brain were performed in Case 1. The phenotypes of both siblings showed marked resemblance to those observed in children with Zellweger syndrome. The results of biochemical tests performed in Case 1, together with abundant peroxisomes in the liver and the wide spectrum of clinical abnormalities suggest pseudo-Zellweger or Zellweger-like syndromes, but no conclusive data have been found. The plasmalogen level in fibroblasts as well as the fibroblasts profile of VLCFA noted in Case 2 were within the normal range, thus excluding the possibility of a peroxisomal disorder. The striking phenotype resemblance of the siblings mimicking Zellweger, together with discordant biochemical findings, are difficult to explain on the basis of currently available tests.

Diagnosis, Differential↗

PubMed2004

Alveolar antioxidant status in patients with acute respiratory distress syndrome.

In the acutely inflamed lung, oxidant stress occurs within the alveolar compartment. Under these conditions, the regulation of low molecular weight antioxidants in the epithelial lining fluid is poorly understood. Therefore, antioxidant levels were measured in the bronchoalveolar lavage fluid (BALF) of patients with acute respiratory distress syndrome (ARDS; n=40) and in healthy volunteers (n=20). Reduced glutathione (GSH), oxidised glutathione (GSSG; enzymatic assay), retinol (vitamin A), alpha-tocopherol (vitamin E), ascorbic acid (vitamin C), uric acid (all by HPLC), plasmalogens (1-alkenyl-2-acyl phospholipids), polyunsaturated fatty acids (PUFA; both by gas-liquid chromatography), and F2-isoprostanes (ELISA) were quantified. All values are expressed as concentrations in cell-depleted BALF. GSSG (ARDS: 0.13+/-0.02 microM; control: 0.03+/-0.01 microM; mean+/-sem) and F2-isoprostanes (ARDS: 78+/-10 pM; control: 26+/-5 pM) were increased in ARDS, thus indicating oxidant stress. GSH levels in patients did not change significantly, whereas concentrations of vitamins A and C, vitamin E (ARDS: 77+/-15 nM; control: 26+/-3 nM) and uric acid (ARDS: 11.8+/-2.2 microM; control: 0.7+/-0.0 microM) were significantly elevated in ARDS. PUFA of total lipids, which may act as sacrificial antioxidants, increased by a factor of approximately 3 in patients, but plasmalogens showed a significant decrease. In conclusion, low molecular weight antioxidants are elevated in the alveolar compartment of patients with acute respiratory distress syndrome. Further research is warranted to elucidate the molecular mechanisms underlying this finding.

Adult↗

PubMed1993

Docosahexaenoic acid--a new therapeutic approach to peroxisomal-disorder patients: experience with two cases.

Docosahexaenoic acid (DHA, 22:6 omega 3) is a major constituent of brain membrane phospholipids and photoreceptor cells. Patients with generalized peroxisomal disorders have extremely low levels of DHA in the brain and other tissues. Since a DHA deficiency could explain some basic symptoms in peroxisomal-disorder patients, we tested the possible beneficial effects of DHA in two patients with neonatal adrenoleukodystrophy (NALD). Before the treatment, both patients had very low DHA levels in plasma and erythrocytes. We first gave DHA in the form of fish oil and, in both patients, the rapid increase in red-cell DHA levels indicated that this fatty acid was being absorbed and incorporated into membrane phospholipids very fast. However, a low ratio 22:6 omega 3/22:5 omega 3 was still present in erythrocyte membranes, and the content of 20:5 omega 3 (eicosapentaenoic acid) was too high with the fish oil diet. We then began treatment with pure DHA ethyl ester and, after a few weeks, erythrocyte omega 3 polyunsaturated fatty acids were normal. There was an increase in the 18:0 molecular species of plasmalogens in both patients, most significantly in the child with affected plasmalogen biosynthesis in cultured fibroblasts. In the less severely affected NALD patient, treatment with DHA produced a very significant decrease in the ratios 24:1/22:0 and 26:1/22:0, and this child improved neurologically. The present data suggest that DHA deficiency may be the cause for some of the most characteristic abnormalities in peroxisomal-disorder patients and open new therapeutic possibilities for these patients.

Child↗

PubMed2003

Membrane phospholipids and high-energy metabolites in childhood ataxia with CNS hypomyelination.

BACKGROUND: Childhood ataxia with CNS hypomyelination (CACH) is a leukodystrophy with extreme rarefaction of white matter caused by mutations in one of the five subunits of the translation initiation factor 2B (eIF2B). METHODS: Seven children with this disease and nine age-matched control subjects were studied with proton-decoupled phosphorus magnetic resonance (MR) spectroscopy. RESULTS: In patients with CACH, cerebral concentrations of high-energy phosphate metabolites were abnormal. Of the metabolites involved in biosynthesis and catabolism of membrane phospholipids, glycerophosphorylethanolamine was reduced (0.24 +/- 0.18 mmol/kg brain vs 0.44 +/- 0.14; p < 0.02), and phosphorylethanolamine was increased (2.32 +/- 0.53 vs 1.53 +/- 0.22; p < 0.01), whereas the choline-containing phosphorylated metabolites were unchanged. Nucleoside triphosphate (NTP) was reduced (2.44 +/- 0.34 mmol/kg brain tissue vs 3.09 +/- 0.58; p < 0.01), phosphocreatine was elevated (4.11 +/- 0.63 vs 3.27 +/- 0.33; p < 0.01), and inorganic phosphate was reduced (0.77 +/- 0.32 vs 1.06 +/- 0.26; p < 0.05). Intracellular pH was elevated in patients (7.03 +/- 0.04 vs 6.99 +/- 0.02; p < 0.02). CONCLUSIONS: The authors found an altered energy state of the residual cell population investigated. Together with previously identified replacement of white matter by CSF, the present findings raise the possibility that the genetic defect in eIF2B may result in impairment of myelin membrane synthesis or myelin membrane transport in the in vivo CACH brain. Ethanolamine metabolites constitute the plasmalogens, and the present findings may include a defect in plasmalogen metabolism.

Adolescent↗

PubMed2000

Therapeutic developments in peroxisome biogenesis disorders.

Clinically, peroxisome biogenesis disorders (PBDs) are a group of lethal diseases with a continuum of severity of clinical symptoms ranging from the most severe form, Zellweger syndrome, to the milder forms, infantile Refsum disease and rhizomelic chondrodysplasia punctata. PBDs are characterised by a number of biochemical abnormalities including impaired degradation of peroxide, very long chain fatty acids, pipecolic acid, phytanic acid and xenobiotics and impaired synthesis of plasmalogens, bile acids, cholesterol and docosahexaenoic acid. Treatment of PBD patients as a group is problematic since a number of patients, especially those with Zellweger syndrome, have significant neocortical alterations in the brain at birth so that full recovery would be impossible even with postnatal therapy. To date, treatment of PBD patients has generally involved only supportive care and symptomatic therapy. However, the fact that some of the milder PBD patients live into the second decade has prompted research into possible treatments for these patients. A number of experimental therapies have been evaluated to determine whether or not correction of biochemical abnormalities through dietary supplementation and/or modification is of clinical benefit to PBD patients. Another approach has been pharmacological induction of peroxisomes in PBD patients to improve overall peroxisomal biochemical function. Well known rodent peroxisomal proliferators were found not to induce human peroxisomes. Recently, our laboratory demonstrated that sodium 4-phenylbutyrate induces peroxisome proliferation and improves biochemical function (very long chain fatty acid beta-oxidation rates and very long chain fatty acid and plasmalogens levels) in fibroblast cell lines from patients with milder PBD phenotypes. Dietary supplementation and/or modification and pharmacological induction of peroxisomes as treatment strategies for PBD patients will be the subject of this review.

Antineoplastic Agents↗

PubMed1977

Phospholipids and phospholipid-bound fatty acids and aldehydes of spermatozoa and seminal plasma of rhesus monkeys.

The major components of the phospholipids of rhesus monkey spermatozoa are phosphatidyl choline (33%), phosphatidyl ethanolamine (25%), ethanolamine plasmalogen (16-1%), sphingomyelin (8-1%), choline plasmalogen (6-9%) and cardiolipin (4-5%). The major phospholipid-bound fatty acids are 16:0, 18:0, 18:1 and 22:6; the major fatty aldehydes are 15:0, 16:0 and 18:2. The same phospholipids are also present in the seminal plasma.

Aldehydes↗

PubMed1996

Meibomian gland phospholipids.

The content of the meibomian gland lipid exprimate is known, but little is known about the phospholipids that comprise the glandular cells. The purpose of the present study is to identify and quantitate the phospholipid complement of the meibomian gland cells that produce the lipid secretion of meibomian oil and which is vital to tear film stability. Eyelids (n = 50) were excised from rabbits, and after surgical removal of surrounding tissues, the tarsal plates with and without expressing meibomian oil were extracted and phospholipids of the plates quantified by 31P nuclear magnetic resonance (NMR). Seventeen phospholipids were quantified from tarsal plates expressed of oil and tarsal plates containing meibomian oil: alkylacylphosphatidylcholine (AAPC), dihydrosphingomyelin (DHSM), dimethylphosphatidylethanolamine, diphosphatidylglycerol (cardiolipin), ethanolamine plasmalogen (EPLAS), lysoethanolamine plasmalogen, lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylserine, phosphatidic acid, phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylglycerol, phosphatidylinositol, phosphatidylserine, sphingomyelin (SM), sphingosylphosphorylcholine. The six zwitterionic and neutral phospholipids, DHSM, EPLAS, PE, SM, AAPC, and PC together comprise 79.5% of the total meibomian gland phospholipid profile (in meibomian oil this value is 84.2%). The zwitterionic and neutral phospholipids dominate meibomian gland phospholipid profiles. Since the meibomian gland cells undergo holocrine secretion and form the meibomian glad secretion, such a composition is consistent with the hypothesis that a chemically stable lamellar surfactant layer phospholipids bind non-polar meibomian oil to the aqueous layer of the tear film.

Animals↗