Temperature-Induced Changes in the Lipid Molecular Species of a Thermophilic Cyanobacterium,Mastigocladus laminosus

1991 ◽  
Vol 55 (3) ◽  
pp. 781-785
Author(s):  
Osamu Hirayama ◽  
Toyomasa Kishida
Keyword(s):  
Molecular Species ◽  
Mastigocladus Laminosus ◽  
Lipid Molecular Species ◽  
Thermophilic Cyanobacterium ◽  
Induced Changes

scholarly journals Diabetes-induced changes in specific lipid molecular species in rat myocardium

2000 ◽  
Vol 352 (1) ◽  
pp. 79 ◽  
Author(s):  
Xianlin HAN ◽  
Dana R. ABENDSCHEIN ◽  
John G. KELLEY ◽  
Richard W. GROSS
Keyword(s):  
Molecular Species ◽  
Rat Myocardium ◽  
Lipid Molecular Species ◽  
Induced Changes ◽  
Specific Lipid

scholarly journals Diabetes-induced changes in specific lipid molecular species in rat myocardium

2000 ◽  
Vol 352 (1) ◽  
pp. 79-89 ◽  
Author(s):  
Xianlin HAN ◽  
Dana R. ABENDSCHEIN ◽  
John G. KELLEY ◽  
Richard W. GROSS
Keyword(s):  
Lipid Metabolism ◽  
Molecular Species ◽  
Insulin Treatment ◽  
Fold Increase ◽  
Acyl Residue ◽  
Individual Molecular Species ◽  
Diabetic State ◽  
Lipid Molecular Species ◽  
Triacylglycerol Molecular Species ◽  
Induced Changes

Intrinsic cardiac dysfunction during the diabetic state has been causally linked to changes in myocardial lipid metabolism. However, the precise alterations in the molecular species of myocardial polar and non-polar lipids during the diabetic state and their responses to insulin have not been investigated. Herein we demonstrate four specific alterations in rat myocardial lipid molecular species after induction of the diabetic state by streptozotocin treatment: (i) a massive remodelling of triacylglycerol molecular species including a > 5-fold increase in tripalmitin mass and a 60% decrease in polyunsaturated triacylglycerol molecular species mass (i.e. triacylglycerols containing at least one acyl residue with more than two double bonds); (ii) a 46% increase in myocardial phosphatidylinositol mass; (iii) a 44% increase in myocardial plasmenylethanolamine mass and (iv) a 22% decrease in 1-stearoyl-2-arachidonoyl phosphatidylethanolamine content. Each of the changes in phospholipid classes, subclasses and individual molecular species were prevented by insulin treatment after induction of the diabetic state. In sharp contrast, the alterations in triacylglycerol molecular species were not preventable by peripheral insulin treatment after induction of the diabetic state. These results segregate diabetes-induced alterations in myocardial lipid metabolism into changes that can be remedied or not by routine peripheral insulin treatment and suggest that peripheral insulin therapy alone may not be sufficient to correct all of the metabolic alterations present in diabetic myocardium.

Testosterone-induced changes in phosphatidylcholine molecular species composition of Plasmodium chabaudi-infected erythrocytes

Parasitology ◽  
1993 ◽  
Vol 107 (5) ◽  
pp. 465-469
Author(s):  
S. Fiebig ◽  
A. P. Simões ◽  
F. Wunderlich ◽  
J. A. F. Op Den Kamp
Keyword(s):  
Species Composition ◽  
Blood Plasma ◽  
Molecular Species ◽  
Phospholipid Class ◽  
Erythrocyte Membranes ◽  
Plasmodium Chabaudi ◽  
Molecular Species Composition ◽  
Testosterone Treatment ◽  
Phospholipid Classes ◽  
Induced Changes

SUMMARYThis study is concerned with the influence of testosterone on the phospholipid class and the phosphatidylcholine molecular species composition of various fractions obtained from the blood of Plasmodium chabaudi-infected mice. Blood plasma, infected erythrocytes, isolated parasites and erythrocyte membranes isolated from both non-infected and infected erythrocytes in the form of ghosts were analysed. In general, the phospholipid classes remained unaffected, while the phosphatidylcholine (PC) molecular species composition showed differences after testosterone treatment. In infected erythrocytes, there was a decrease in 16:0/20:4-PC and 18:0/20:4-PC and an increase in 16:0/18:2(16:0/20:3)-PC. The decrease of 16:0/20:4-PC was exclusively confined to parasites. The rise in 16:0/18:2(16:0/20: 3)-PC and the diminution of 18:0/20:4-PC occurred in the erythrocyte membrane of both infected ghosts and non-infected ghosts as well as in the blood plasma. It is suggested that these changes occur primarily in the plasma thereby influencing the erythrocyte membranes. The decrease in 16:0/20:4-PC supports the view of the independence of the parasite from the biosynthetic lipid pathways of its host cell.

scholarly journals Oestradiol-induced changes in the composition of phospholipid classes of quail oviduct: specific replacement of arachidonic acid by docosahexaenoic acid in alkenylacyl-glycerophosphoethanolamine

1994 ◽  
Vol 301 (2) ◽  
pp. 361-366 ◽  
Author(s):  
B E Felouati ◽  
J F Pageaux ◽  
J M Fayard ◽  
M Lagarde ◽  
C Laugier
Keyword(s):  
Cell Proliferation ◽  
Arachidonic Acid ◽  
Molecular Species ◽  
Phospholipid Composition ◽  
Oestrogen Treatment ◽  
Ethanolamine Glycerophospholipids ◽  
Striking Result ◽  
Choline Glycerophospholipids ◽  
Phospholipid Classes ◽  
Induced Changes

The phospholipid composition and the molecular species of the major subclasses of ethanolamine and choline glycerophospholipids were determined during the natural or oestradiol-induced development of the quail oviduct. The phospholipid concentration increased significantly during oviduct development, and the proportion of ethanolamine glycerophospholipids (EPL) remained constant while that of choline glycerophospholipids increased. The immature oviduct contained the majority of its endogenous arachidonic acid mass (71%) in EPL, mainly in alkenylacyl-glycerophosphoethanolamine (alkenylacyl-GPE) (49% of the total). Oestrogen treatment induced the depletion of 20:4,n-6 specifically from this pool, which indicates the biological importance of 20:4,n-6 molecular species in alkenylacyl-GPE as substrates for the oviduct phospholipases activated by oestradiol, and suggests that this EPL subclass is involved in the oestrogen-induced cell proliferation. Another striking result was the marked increase in 22:6,n-3 EPL molecular species following the oestradiol treatment and more particularly the strict substitution of 20:4,n-6 by 22:6,n-3 in alkenylacyl-GPE. We speculate that alkenylacyl-GPE molecular species containing 22:6,n-3 may participate in the arrest of oestrogen-induced proliferation.

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