Clofibric acid increases molecular species of phosphatidylethanolamine containing arachidonic acid for biogenesis of peroxisomal membranes in peroxisome proliferation in the liver

Author(s):  
Hiroaki Miura ◽  
Hiroki Mizuguchi ◽  
Mino Amano-Iwashita ◽  
Rie Maeda-Kogure ◽  
Akio Negishi ◽  
...  
1992 ◽  
Vol 43 (11) ◽  
pp. 2321-2326 ◽  
Author(s):  
Yoichi Kawashima ◽  
Hiromi Nishizawa ◽  
Hiroshi Kozuka

1994 ◽  
Vol 301 (2) ◽  
pp. 361-366 ◽  
Author(s):  
B E Felouati ◽  
J F Pageaux ◽  
J M Fayard ◽  
M Lagarde ◽  
C Laugier

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.


Author(s):  
Charles L. Swendsen ◽  
Floyd H. Chilton ◽  
Joseph T. O'Flaherty ◽  
Jefferson R. Suries ◽  
Claude Piantadosi ◽  
...  

1989 ◽  
Vol 66 (6) ◽  
pp. 2763-2771 ◽  
Author(s):  
F. H. Chilton ◽  
J. Y. Westcott ◽  
L. M. Zapp ◽  
J. E. Henson ◽  
N. F. Voelkel

This study has attempted to identify the cells and phosphoglyceride molecular species associated with the rapid turnover of arachidonic acid (AA) in the isolated rat lung. In initial studies, AA complexed to trace amounts of albumin was added to the perfusate of rat lungs for 15 min and the incorporation of [3H]AA into various cells and phosphoglyceride molecular species was determined. Autoradiographic analysis revealed that the AA had labeled endothelial cells but also had already escaped from the intravascular space and labeled epithelial cells including alveolar type II cells. In addition, [3H]AA was found to be incorporated into various phosphoglycerides: phosphatidylcholine (PC) greater than phosphatidylethanolamine (PE) greater than phosphatidylinositol (PI). The majority of this [3H]AA was incorporated into 1-acyl-2-arachidonoyl-sn-glycero-3-PC, -PE, and -PI during the 15-min labeling period. In subsequent experiments, AA remodeling in the lung was examined by pulse labeling with [3H]AA for 15 min, washing unbound AA with albumin, and perfusing for an additional 120 min. In these lungs, some of the [3H]AA was remodeled into 1-alk-1-enyl-acyl-sn-glycero-3-PE. Gas chromatography-mass spectrometry analysis revealed that the largest pools of endogenous AA in the lung are found in PE associated with 1-alk-1-enyl-linked molecular species. On ionophore stimulation of lungs labeled for 15 min, labeled leukotriene (LT) B4, leukotriene C4, and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were produced. LTC4 had a profoundly different radiospecific activity compared with LTB4 and 6-keto-PGF1 alpha, suggesting a different source of AA as contributing to the production of this eicosanoid.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document