scholarly journals Phospholipid transfer between plasma and platelets in vitro

Blood ◽  
1976 ◽  
Vol 48 (2) ◽  
pp. 199-211 ◽  
Author(s):  
JH Joist ◽  
G Dolezel ◽  
JV Lloyd ◽  
F Mustard

Abstract Washed rabbit platelets were resuspended in plasma in which all of the major phospholipids had been isotopically labeled by injection of 32PO4 into rabbits. At certain time intervals during a 6-hr incubation at 37 degrees C, aliquots were removed from the incubation mixture and the platelets were isolated and subjected to lipid extraction and phospholipid analysis. A continuous rise in platelet non-lipid-bound and lipid-bound radioactivity was observed through-out the incubation period. Two platelet phospholipids, lecithin and lysolecithin, were significantly labeled, whereas little or no labeling of the other phospholipids was found. There was no detectable change in total or individual platelet phospholipid content. At 6 hr, 4% of total platelet phospholipid, 43% of platelet lysolecithin, and 7% of platelet lecithin were labeled. Platelets incubated in plasma from rabbits with diet- induced hyperlipidemia took up and incorporated significantly more label into their phospholipids than did platelets in normal plasma. Labeling of both platelet lysolecithin and lecithin could be due to uptake and metabolism of plasma lysolecithin by platelets. However, labeling of platelet lecithin could at least in part be the result of direct exchange of this phospholipid with the plasma. Uptake and incorporation of endogenous plasma lysolecithin by platelets and, possibly, direct exchanged of platelet lecithin may be important mechanisms in the modification by plasma lipids of platelet membrane phospholipid fatty acid composition and platelet function.

Blood ◽  
1976 ◽  
Vol 48 (2) ◽  
pp. 199-211
Author(s):  
JH Joist ◽  
G Dolezel ◽  
JV Lloyd ◽  
F Mustard

Washed rabbit platelets were resuspended in plasma in which all of the major phospholipids had been isotopically labeled by injection of 32PO4 into rabbits. At certain time intervals during a 6-hr incubation at 37 degrees C, aliquots were removed from the incubation mixture and the platelets were isolated and subjected to lipid extraction and phospholipid analysis. A continuous rise in platelet non-lipid-bound and lipid-bound radioactivity was observed through-out the incubation period. Two platelet phospholipids, lecithin and lysolecithin, were significantly labeled, whereas little or no labeling of the other phospholipids was found. There was no detectable change in total or individual platelet phospholipid content. At 6 hr, 4% of total platelet phospholipid, 43% of platelet lysolecithin, and 7% of platelet lecithin were labeled. Platelets incubated in plasma from rabbits with diet- induced hyperlipidemia took up and incorporated significantly more label into their phospholipids than did platelets in normal plasma. Labeling of both platelet lysolecithin and lecithin could be due to uptake and metabolism of plasma lysolecithin by platelets. However, labeling of platelet lecithin could at least in part be the result of direct exchange of this phospholipid with the plasma. Uptake and incorporation of endogenous plasma lysolecithin by platelets and, possibly, direct exchanged of platelet lecithin may be important mechanisms in the modification by plasma lipids of platelet membrane phospholipid fatty acid composition and platelet function.


2014 ◽  
pp. 331-339
Author(s):  
S. PETROVIĆ ◽  
M. TAKIĆ ◽  
A. ARSIĆ ◽  
V. VUČIĆ ◽  
D. DRAKULIĆ ◽  
...  

The effects of 8-days treatment with 17α-estradiol (33.3 µg/kg) and progesterone (1.7 mg/kg) on plasma lipids and fatty acid composition of plasma phospholipids were examined in intact (INT) and bilaterally common carotid arteries occluded (BCO) male Wistar rats. Significant decrease of triglyceride level was found in BCO rats after the estradiol treatment. Both hormones elevated proportion of 18:1n-7 fatty acid in INT, but they failed to have such an effect in BCO. Estradiol increased 22:5n-3 and total n-3 polyunsaturated fatty acids (PUFA) in intact, and decreased 18:2n-6 in BCO rats. Significantly lower level of total n-3 was found in progesterone-treated than in estradiol-treated BCO rats. Given that n-3 PUFA have many beneficial effects on cell and tissue function, while n-6 PUFA have mostly the opposite effects, estradiol, rather than progesterone, was seen to improve plasma lipids and phospholipids FA profiles in INT and BCO animals. Estradiol significantly elevated the estimated activity of Δ9-desaturases and progesterone of Δ5-desaturase in BCO group, with no effects in INT rats.


Platelets ◽  
1996 ◽  
Vol 7 (1-2) ◽  
pp. 69-73 ◽  
Author(s):  
D. Prisco ◽  
R. Paniccia ◽  
B. Bandinelli ◽  
M. Filippini ◽  
I. Francalanci ◽  
...  

1977 ◽  
Author(s):  
R.A. Hutton ◽  
R.M. Hardisty

In vitro incorporation of glycerol-2-3H into phospholipids of normal platelets was measured at rest and during platelet aggregation induced by adenosine diphosphate, epinephrine, collagen and ristocetin. Compared to the basal state, aggregating platelets showed a marked increase in total glycerol uptake, although total platelet phospholipid content was unchanged. The most striking change was an increase in the proportion of the radioactivity incorporated into the phosphatidyl inositol fraction (from 11% to 36% after 30 minutes incubation with epinephrine), this being largely at the expense of the phosphatidyl choline fraction which decreased from 46% to 30%. The extent of the glycerol uptake correlated well with the degree of platelet aggregation observed (p = 0.05 for adenosine diphosphate), but was not directly related to the speed of either aggregation or the release reaction. The rate of glycerol uptake paralleled the development of platelet factor 3 availability (PF3a) over the first 20-30 minutes of incubation, but thereafter, PF3a levelled off while glycerol uptake continued to rise for at least another 30 minutes. We conclude that the changes in platelet phospholipid turnover observed here during platelet aggregation, are of little direct consequence to the cells haemostatic functions. The increase in phosphatidyl inositol turnover may represent part of the cells’ response to membrane distortion or damage during the secretory process, as has been documented in other secretory processes.


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