Reversible reduction of phospholipid bound arachidonic acid after low density lipoprotein apheresis. Evidence for rapid incorporation of plasmalogen phosphatidylethanolamine into the red blood cell membrane

Engelmann, Bernd; Bräutigam, Carola; Kulschar, Robert; Duhm, Jochen; Prenner, Elmar J.; Hermetter, Albin; Richter, Werner; Thiery, Joachim; Seidel, D.

doi:10.1016/0005-2736(94)00227-4

Cited by 19 publications

(8 citation statements)

References 32 publications

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“…Plasmalogen phospholipids have been demonstrated to play a significant role in the defense of LDL particles against oxidative stress [81]. As we have found lower levels of erythrocyte plasmalogen phospholipids in malnourished compared to well-nourished predialysis patients, one could speculate that an increased oxidative stress might be a contributing factor to the high prevalence of CVD documented in malnourished and inflamed CRF patients [82].…”

Section: Does Inflammation Cause Increased Oxidative Stress?mentioning

confidence: 62%

Malnutrition and Chronic Inflammation as Risk Factors for Cardiovascular Disease in Chronic Renal Failure

Stenvinkel

2000

Blood Purif

133

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Section: Does Inflammation Cause Increased Oxidative Stress?mentioning

confidence: 62%

Malnutrition and Chronic Inflammation as Risk Factors for Cardiovascular Disease in Chronic Renal Failure

Stenvinkel

2000

Blood Purif

133

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“…The plasmalogen concentration in the blood cells was 20 times higher than that in the blood plasma (Figs. 3A and 3C), and it was reported that phospholipids in the plasma are rapidly incorporated into the red blood cell membrane (13). These results suggest that blood cell plasmalogen is maintained at a constant level.…”

Section: Discussionmentioning

confidence: 78%

“…Several studies have shown that dietary alkylacylglycerol, another ether-linked lipid, is absorbed and incorporated as plasmalogen in tissues and red blood cell membranes (13), and alkylacylglycerol supplementation was found to restore tissue plasmalogen deficiency (14). However, no data have been reported on the absorption of dietary alkenyl phospholipids or plasmalogen, nor are data available on the fate of plasmalogen vinyl ether double bonds after the ingestion of foods that are common sources of plasmalogens (15).…”

mentioning

confidence: 99%

Ingestion of plasmalogen markedly increased plasmalogen levels of blood plasma in rats

Nishimukai

Wakisaka

Hara

2003

Lipids

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Plasmalogens, a subclass of phospholipids, are widely distributed in human and animals, and are taken into the body as food. However, no data exist on the intestinal absorption or fate of ingested plasmalogen. Here, we determined whether dietary plasmalogen is absorbed and whether blood and tissue concentrations increased in normal male Wistar rats by using four separate experiments. Phospholipids containing more than 20 wt% of plasmalogen extracted from the bovine brain were incorporated into test diets (10-15 wt%). In experiment 1, we estimated the absorption rate by measuring the plasmalogen vinyl ether bonds remaining in the alimentary tract of rats after the ingestion of 2 g of test diet containing 91 micromol plasmalogen. The absorption rate of plasmalogen was nearly 80 mol% after 4 h, comparable to the total phospholipid content in the test diet. In experiment 2, we observed no degradation of the plasmalogen vinyl ether bonds under in vitro conditions simulating those of the stomach and small intestinal lumen. In experiment 3 we confirmed a comparable absorption (36 mol%) by using a closed loop of the upper small intestine in anesthetized rats 90 min after injecting a 10 wt% brain phospholipid emulsion. Feeding a test diet containing 10 wt% brain phospholipids for 7 d increased plasmalogen concentration threefold in blood plasma and by 25% in the liver; however, no increases were seen in blood cells, skeletal muscle, brain, lungs, kidneys, or adipose tissue (experiment 4). We concluded that dietary plasmalogen is absorbed from the intestine and contributes to a large increase in plasmalogen levels in blood plasma.

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“…Plasmalogens were shown to be rapidly exchanged between lipid donors and erythrocytes. 48 The plasmalogen pool of red blood cells, LDL from normolipidemic individuals was enriched in vitro with 3 different amounts of plasmenylethanolamine or diacyl PE as described in Methods. Subsequently, the modified particles were oxidized with CuCl 2 (1.67 nmol/ml) for maximally 4 h and the lag time values measured.…”

Section: Discussionmentioning

confidence: 99%

Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

Hahnel¹,

Thiery²,

Brosche³

et al. 1999

ATVB

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Extracorporeal reduction of plasma low density lipoproteins (LDLs) by LDL apheresis was shown to attenuate the proatherogenic influences of LDL, such as impairment of vasodilation and increased monocyte adhesion to the endothelium. In 16 patients with familial hypercholesterolemia, we analyzed whether LDL apheresis by the heparin precipitation procedure affected the oxidative resistance of LDL. Plasma LDL cholesterol concentrations were reduced by 65% after the apheresis. The lag time of copper-mediated LDL oxidation was increased from 103 to 117 minutes (P<0.0005). The LDL contents of alpha-tocopherol and beta-carotene, as well as the ratio of monounsaturated to polyunsaturated fatty acids in LDL, were not altered. However, the LDL apheresis induced a 15% increase in the LDL contents of plasmalogen phospholipids (P<0.0005), a class of ether phospholipids that were recently shown to prevent lipid oxidation. The phosphatidylcholine (PC) to lysoPC ratio was elevated by 16% after the apheresis (P<0.0005). The percent increase in LDL plasmalogen phospholipids showed a close association with the increased lag time after apheresis (P<0.0005). The LDL plasmalogen contents of the blood samples from patients and from normolipidemic donors were also positively related to the lag time (P<0.005). In vitro loading of LDL with plasmalogen phospholipids resulted in a prolongation of the lag time and an increase in the PC/lysoPC ratio. In conclusion, the rapid rise in LDL contents of plasmalogen phospholipids most probably causes the increase in lag time after LDL apheresis. Plasmalogens appear to play an important role in the oxidation resistance of LDL in vivo.

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Reversible reduction of phospholipid bound arachidonic acid after low density lipoprotein apheresis. Evidence for rapid incorporation of plasmalogen phosphatidylethanolamine into the red blood cell membrane

Cited by 19 publications

References 32 publications

Malnutrition and Chronic Inflammation as Risk Factors for Cardiovascular Disease in Chronic Renal Failure

Malnutrition and Chronic Inflammation as Risk Factors for Cardiovascular Disease in Chronic Renal Failure

Ingestion of plasmalogen markedly increased plasmalogen levels of blood plasma in rats

Role of Plasmalogens in the Enhanced Resistance of LDL to Copper-Induced Oxidation After LDL Apheresis

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