Phospholipase A2 in rat-lung microsomes: Substrate specificity towards endogenous phosphatidylcholines

Longmore, William J.; Oldenburg, V.; Golde, L.M.G. Van

doi:10.1016/0005-2760(79)90152-8

Cited by 70 publications

(12 citation statements)

References 33 publications

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“…The resulting lysoPC can be reacylated with acyl-CoA esters, as first described by Lands (Lands 1958(Lands , 1960. The necessary enzyme is reported to be present in lung (Lands 1960;Garcia et al 1975;Longmore et al 1979;Ohta et al 1972). One factor in the decrease of sn-1 lysoPCs may be explained by the remodeling pathway (Lands' cycle).…”

Section: Biomarkers Related To Lung Cancermentioning

confidence: 95%

Lysophosphatidylcholine profiling of plasma: discrimination of isomers and discovery of lung cancer biomarkers

et al. 2010

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Lysophosphatidylcholines (lysoPCs) are a class of compounds that have a constant polar head, and fatty acyls of different chain lengths, position, degrees of saturation, and double bond location in human plasma. LysoPCs levels can be a clinical diagnostic indicator that reveals pathophysiological changes. In this work, a method was developed to discriminate between different types of lysoPCs using reversed phase ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry, using mass spectrometry MS E . Isomeric lysoPCs were distinguished based on retention time and the peak intensity ratio of product ions, and 14 pairs of lysoPCs regioisomers were identified in human plasma. The plasma samples of 12 lung cancer patients and 12 healthy persons were collected and analyzed by principal component analysis to generate metabolic profiles of the identified lysoPCs. Both electrospray ionization ESI? and ESIresults showed that all lung cancer patients had the same five lysoPC metabolic abnormalities, specifically in sn-1 lyso16:0, sn-2 lysoPC 16:0, sn-1 lysoPC 18:0, sn-1 lysoPC 18:1 and sn-1 lysoPC 18:2. Thus, the function of isomers with different fatty acyl positions may be related to lung cancer, and this may help elucidate the mechanism of the disease.

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Section: Biomarkers Related To Lung Cancermentioning

confidence: 95%

Lysophosphatidylcholine profiling of plasma: discrimination of isomers and discovery of lung cancer biomarkers

et al. 2010

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“…The first enzymatic reaction in the remodeling pathway is the deacylation of PC by PLA 2 . Numerous PLA 2 isoforms exist in the mammalian genome (47,48), and PLA 2 activity has been localized to distinct subcellular compartments of the lung, including cytosol, microsomes, lysosomes, and lamellar bodies (49)(50)(51)(52)(53)(54)(55)(56). PRDX6 is a Ca 2+ -independent, acidic PLA 2 that localizes to lysosomes and lamellar bodies and is a dual-function enzyme with peroxidase and phospholipase activity (57).…”

Section: Figurementioning

confidence: 99%

LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice

Bridges¹,

Ikegami²,

Brilli³

et al. 2010

J. Clin. Invest.

134

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Respiratory distress syndrome (RDS), which is the leading cause of death in premature infants, is caused by surfactant deficiency. The most critical and abundant phospholipid in pulmonary surfactant is saturated phosphatidylcholine (SatPC), which is synthesized in alveolar type II cells de novo or by the deacylation-reacylation of existing phosphatidylcholine species. We recently cloned and partially characterized a mouse enzyme with characteristics of a lung lysophosphatidylcholine acyltransferase (LPCAT1) that we predicted would be involved in surfactant synthesis. Here, we describe our studies investigating whether LPCAT1 is required for pulmonary surfactant homeostasis. To address this issue, we generated mice bearing a hypomorphic allele of Lpcat1 (referred to herein as Lpcat1 GT/GT mice) using a genetrap strategy. Newborn Lpcat1 GT/GT mice showed varying perinatal mortality from respiratory failure, with affected animals demonstrating hallmarks of respiratory distress such as atelectasis and hyaline membranes. Lpcat1 mRNA levels were reduced in newborn Lpcat1 GT/GT mice and directly correlated with SatPC content, LPCAT1 activity, and survival. Surfactant isolated from dead Lpcat1 GT/GT mice failed to reduce minimum surface tension to wild-type levels. Collectively, these data demonstrate that full LPCAT1 activity is required to achieve the levels of SatPC essential for the transition to air breathing.

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“…Microsomal phospholipase A activity was measured by endogenously labelled PC (Longmore et al, 1979).…”

Section: Assay Of Microsomal Phospholipase A;mentioning

confidence: 99%

Changes in lipid profiles of liver microsomes of rats following intratracheal administration of DDT or endosulfan

Narayan¹,

Dani²,

Misra³

1990

J. of Env. Sc. & Hlth., Part B

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The effect of intratracheal administration of DDT (5 mg/100 g body weight) or endosulfan (1 mg/100 g body weight) to rats for three consecutive days, has been studied on liver lipid metabolism. The administration of DDT but not endosulfan significantly increased the liver weight and the microsomal protein contents. Both DDT and endosulfan treatments significantly increased the contents of microsomal phosphatidylcholine (PC), total-free- and esterified cholesterol. The distribution of unsaturated fatty acids of microsomal PC and PE was increased by DDT treatment. The intratracheal administration of DDT caused fatty infiltration of liver which was probably due to increased synthesis of triglycerides (TG). This is supported by the increased incorporation of radioactive palmitate-1-14C into microsomal TG. However, the increased incorporation of palmitate-1-14C into microsomal PC and phosphatidylethanolamine (PE) after the DDT treatment, was due to the increased transacylation reaction supported by the decreased activity of microsomal phospholipase A. The intratracheal administration of endosulfan did not have pronounced effect on liver fatty infiltration, or transacylation reaction in microsomal PC and PE. However, the results have shown that the treatments of DDT or endosulfan increased the PC contents and the incorporation of radioactive [methyl-3H]choline into PC of microsomes, resulting the increased synthesis of PC via CDPcholine pathway. Thus, the intratracheally administered DDT or endosulfan to rats showed that both the insecticides cause manifestations in the biochemistry of microsomal membrane lipids, although the effects of DDT being more pronounced. Therefore, the translocation effects of these insecticides or metabolites from lung to liver is established.

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Phospholipase A2 in rat-lung microsomes: Substrate specificity towards endogenous phosphatidylcholines

Cited by 70 publications

References 33 publications

Lysophosphatidylcholine profiling of plasma: discrimination of isomers and discovery of lung cancer biomarkers

Lysophosphatidylcholine profiling of plasma: discrimination of isomers and discovery of lung cancer biomarkers

LPCAT1 regulates surfactant phospholipid synthesis and is required for transitioning to air breathing in mice

Changes in lipid profiles of liver microsomes of rats following intratracheal administration of DDT or endosulfan

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