Lactacystin stimulates arachidonic acid metabolism in rat liver cells: effects of cell density on arachidonic acid release, PGI2production and cyclooxygenase activity

2000 ◽  
Vol 63 (6) ◽  
pp. 371-375 ◽  
Author(s):  
L. Levine
Keyword(s):  
Arachidonic Acid ◽  
Cell Density ◽  
Rat Liver ◽  
Acid Metabolism ◽  
Liver Cells ◽  
Arachidonic Acid Metabolism ◽  
Arachidonic Acid Release ◽  
Cyclooxygenase Activity ◽  
Rat Liver Cells ◽  
Acid Release

scholarly journals The influence of albumin and calcium on human platelet arachidonic acid metabolism

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 418-423 ◽  
Author(s):  
MJ Stuart ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Arachidonic Acid Metabolism ◽  
Albumin Concentration ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
External Calcium ◽  
Platelet Thromboxane

Abstract The effects of in vitro changes in calcium and albumin on human platelet arachidonic acid metabolism were evaluated. Hypoalbuminemia enhanced the conversion of released 14C-arachidonic acid from prelabeled platelet phospholipids to the metabolites of the platelet cyclooxygenase and lipoxygenase pathways. This effect was, however, associated with a decreased release of arachidonic acid in the presence of hypoalbuminemia, such that the overall conversion of released 14C- arachidonic acid to platelet thromboxane B2 was similar in the presence of physiologic albumin concentration (3.5 g/dl) or at decreased albumin concentrations of 0.7 and 0.0 g/dl. External calcium was shown to be important for optimal platelet arachidonic acid release, with maximal release occurring at 1 mM calcium.

scholarly journals The influence of albumin and calcium on human platelet arachidonic acid metabolism

Blood ◽  
1980 ◽  
Vol 55 (3) ◽  
pp. 418-423
Author(s):  
MJ Stuart ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Human Platelet ◽  
Arachidonic Acid Metabolism ◽  
Albumin Concentration ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
External Calcium ◽  
Platelet Thromboxane

The effects of in vitro changes in calcium and albumin on human platelet arachidonic acid metabolism were evaluated. Hypoalbuminemia enhanced the conversion of released 14C-arachidonic acid from prelabeled platelet phospholipids to the metabolites of the platelet cyclooxygenase and lipoxygenase pathways. This effect was, however, associated with a decreased release of arachidonic acid in the presence of hypoalbuminemia, such that the overall conversion of released 14C- arachidonic acid to platelet thromboxane B2 was similar in the presence of physiologic albumin concentration (3.5 g/dl) or at decreased albumin concentrations of 0.7 and 0.0 g/dl. External calcium was shown to be important for optimal platelet arachidonic acid release, with maximal release occurring at 1 mM calcium.

Reduced prostacyclin formation after reoxygenation of anoxic endothelium

1990 ◽  
Vol 259 (5) ◽  
pp. C738-C745 ◽  
Author(s):  
S. L. Hempel ◽  
D. L. Haycraft ◽  
J. C. Hoak ◽  
A. A. Spector
Keyword(s):  
Arachidonic Acid ◽  
Umbilical Vein ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
High Rate ◽  
Ionophore A23187 ◽  
Arachidonic Acid Release ◽  
Cyclooxygenase Activity ◽  
Platelet Adherence ◽  
Acid Release

Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesting that cyclooxygenase activity, but not prostacyclin synthase, is affected by reoxygenation. A decrease in arachidonic acid release from cellular lipids also occurred. The reduction in cyclooxygenase activity, but not arachidonic acid release, was prevented by the presence of ibuprofen during reoxygenation. Addition of catalase or superoxide dismutase during reoxygenation increased PGI2 release but did not completely overcome the reduction relative to control cultures. These findings suggest that the increase in platelet adherence during reoxygenation may be mediated in part by a change in cyclooxygenase activity. This is only partly overcome by extracellular oxygen species scavengers but is prevented by the presence of a reversible cyclooxygenase inhibitor during reoxygenation.

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