Negative allometry of docosahexaenoic acid in the fowl lung and pulmonary surfactant phospholipids

2012 ◽  
Vol 63 (2) ◽  
pp. 202-217 ◽  
Author(s):  
A. Szabó ◽  
M. Mézes ◽  
K. Balogh ◽  
R. Romvári ◽  
P. Horn ◽  
...  
2007 ◽  
Vol 140 (3) ◽  
pp. 117-124 ◽  
Author(s):  
Lian Li ◽  
Hua She ◽  
Shao-Jie Yue ◽  
Xiao-Qun Qin ◽  
Cha-Xiang Guan ◽  
...  

PEDIATRICS ◽  
1979 ◽  
Vol 63 (6) ◽  
pp. 855-859
Author(s):  
Zvi Friedman ◽  
Abraham Rosenberg

A low-birth-weight infant, suffering from chronic bronchopulmonary dysplasia following hyaline membrane disease and recurrent episodes of necrotizing enterocolitis, developed biochemical evidence of essential fatty acid (EFA) deficiency in the plasma. Fatty acid composition of phosphatidylcholine and phosphatidylglycerol in the lung lavage fluid was abnormal. Plasma changes includcd a decrease in the level of linoleic acid and an increased level of palmitic, palmitoleic, oleic, and 5,8, 11-eicosatrienoic acids, the ratio of 5,8,11-eicosatrienoic acid to arachidonic acid being > 0.4:1. A lower than normal level of palmitic acid and an increased level of palmitoleic and oleic acids were seen in pulmonary surfactant phospholipid components. Upon treatment and recovery from EFA deficiency, the fatty acid pattern both in plasma and surfactant phospholipids returned to normal along with clinical improvement. An association between EFA deficiency and altered fatty acid composition of pulmonary surfactant phospholipids is suggested.


1992 ◽  
Vol 51 (4) ◽  
pp. 379-385 ◽  
Author(s):  
Hiroshi Hayakawa ◽  
Girish Giridhar ◽  
Quentin N. Myrvik ◽  
Louis Kucera

1999 ◽  
Vol 277 (6) ◽  
pp. L1179-L1189 ◽  
Author(s):  
Kaushik Nag ◽  
James G. Munro ◽  
Kevin Inchley ◽  
Samuel Schürch ◽  
Nils O. Petersen ◽  
...  

Pulmonary surfactant stabilizes the alveoli by lining the air-fluid interface with films that reduce surface tension to near 0 mN/m (γmin). Surfactant protein B (SP-B) enhances the surface activity of surfactant phospholipids. A captive bubble tensiometer (CBT) was used to study the properties of adsorbed films of dipalmitoylphosphatidylcholine (DPPC) with acidic 1-palmitoyl-2-oleoyl- sn-glycero-3-[phospho- rac-(1-glycerol)] (POPG) or neutral 1-palmitoyl-2-oleoyl- sn-glycerol-3-phosphocholine with (7:3) and without 1% dimeric SP-B. SP-B enhanced the adsorption rate of DPPC-containing neutral or acidic lipid suspensions (1 mg/ml) to a similar extent. Quasi-static cycling of these films revealed that SP-B significantly decreased the film area reduction required to reach γmin for the acidic but not for the neutral system. The results obtained with DPPC-phosphatidylglycerol (PG)-SP-B were consistent with selective DPPC adsorption into the surface monolayer during film formation. Film area reduction required to reach γmin with this system (with and without calcium) approached that of pure DPPC, suggesting selective DPPC insertion and PG squeeze-out. Dynamic cycling of such films showed that larger film area reductions were required to reach γmin for the neutral than for acidic system, even after 20 cycles. Fluorescence microscopy of solvent-spread DPPC-POPG-SP-B planar films revealed highly condensed structures at ∼25 mN/m, although no specific PG phase-segregated structures could be identified. The study suggests that specific interactions of SP-B with acidic phospholipids of surfactant may be involved in the generation and maintenance of DPPC-rich films in the alveoli.


2002 ◽  
Vol 283 (5) ◽  
pp. L1079-L1085 ◽  
Author(s):  
R. Schmidt ◽  
U. Meier ◽  
P. Markart ◽  
F. Grimminger ◽  
H. G. Velcovsky ◽  
...  

Deterioration of pulmonary surfactant function has been reported in interstitial lung disease; however, the molecular basis is presently unclear. We analyzed fatty acid (FA) profiles of several surfactant phospholipid classes isolated from large-surfactant aggregates of patients with idiopathic pulmonary fibrosis (IPF; n = 12), hypersensitivity pneumonitis ( n = 5), and sarcoidosis ( n = 12). Eight healthy individuals served as controls. The relative content of palmitic acid in phosphatidylcholine was significantly reduced in IPF (66.8 ± 2.5%; means ± SE; P < 0.01) but not in hypersensitivity pneumonitis (78.5 ± 1.8%) and sarcoidosis (78.2 ± 3.1%; control 80.1 ± 0.7%). In addition, the phosphatidylglycerol FA profile was significantly altered in the IPF patients, with a lower relative content of its major FA, oleic acid, at the expense of saturated FA. In the phosphatidylcholine class, a significant correlation between the impairment of biophysical surfactant function and decreased percentages of palmitic acid was noted. We conclude that significant alterations in the FA profile of pulmonary surfactant phospholipids occur predominantly in IPF and may contribute to the disturbances of alveolar surface activity in this disease.


1983 ◽  
Vol 245 (5) ◽  
pp. C397-C404 ◽  
Author(s):  
A. Chander ◽  
W. D. Claypool ◽  
J. F. Strauss ◽  
A. B. Fisher

Reuptake of pulmonary surfactant phospholipids was investigated with rat granular pneumocytes in primary culture and L-alpha-[2-palmitoyl-9,10-3H]dipalmitoyl phosphatidylcholine:egg phosphatidylcholine:phosphatidylglycerol:cholesterol (10:5:2:3, mol/mol) liposomes. Uptake of liposomal phosphatidylcholine by granular pneumocytes increased with time and concentration of phosphatidylcholine in the medium. With 150 microM phosphatidylcholine, uptake was about 5 nmol/mg cell protein in 2 h. Phosphatidylcholine uptake was in large part due to net transfer of vesicles as indicated by uptake of [14C]sucrose encapsulated in the aqueous compartment of liposomes. Using dipalmitoyl phosphatidylcholine:cholesterol (1:1) liposomes, uptake was inhibited significantly at 26 degrees C and completely at 4 degrees C. Inhibitors and uncouplers of oxidative phosphorylation had no effect on uptake although uptake was somewhat inhibited in the presence of either 5.6 mM 2-deoxy-D-glucose or 10 mM sodium fluoride. Cell-associated lipid radioactivity decreased after treatment with 0.25% trypsin. The percent radioactivity that was trypsin releasable decreased with increasing time and phosphatidylcholine concentration. The results suggest that uptake of phospholipids by these cells is by surface binding followed by internalization. After 2 h of incubation, 65.3 +/- 3.1% of the cell-associated radioactivity was present in phosphatidylcholine, a small fraction in phosphatidylglycerol, and the remainder in lysophosphatidylcholine, free fatty acids, and other neutral lipids, suggesting metabolic degradation of internalized lipids. This process of phospholipid uptake and degradation may have a physiological role in metabolism of surfactant phospholipids in the lung.


2005 ◽  
Vol 89 (1) ◽  
pp. 306-314 ◽  
Author(s):  
Wenfei Yan ◽  
Barbora Piknova ◽  
Stephen B. Hall

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