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M Croset

Publications and source records attributed to M Croset.

At least 37 records · Page 2Linked to original sources
PubMed1991

12-HETE inhibits the binding of PGH2/TXA2 receptor ligands in human platelets.

12(S)-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE), the end-lipoxygenase product of arachidonic acid in platelets has been previously shown to prevent PGH2/TxA2-induced aggregation. From the present study, we show that 12-HETE inhibits the binding of [125I]-PTA-OH, a thromboxane antagonist, to platelet membranes with an IC50 of 8 microM. This value is in accordance with previously reported 12-HETE concentrations required to prevent the aggregation induced by TxA2 mimetics, the methano analogues of PGH2, U44069 and U46619. When [3H]-U44069 was used as a thromboxane agonist to label intact platelets, 12-HETE also inhibited its binding. We conclude that part of the inhibitory effect of 12-HETE on PGH2/TxA2-induced aggregation might be the result of interacting with PGH2/TxA2 receptor sites.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1991

Leukotriene B4 level in neutrophils from allergic and healthy subjects stimulated by low concentration of calcium ionophore A23187. Effect of exogenous arachidonic acid and possible endogenous source.

Peripheral blood neutrophils from patients with allergic rhinitis and from normal subjects were incubated for 5 min at 37 degrees C with 0.15 microM calcium ionophore A23187 in the absence or presence of exogenous arachidonic acid (2.5 to 10 microM). In neutrophils from allergic patients, the leukotriene B4 (LTB4) level was significantly increased by exogenous arachidonic acid in a concentration-dependent manner (16.2 +/- 4.2 and 38.1 +/- 6.8 pmol/5 min per 2 X 10(6) cells in the absence and presence of 10 microM arachidonic acid, respectively; P less than 0.005; n = 8). The LTB4 level in neutrophils from healthy subjects was only 0.97 +/- 0.17 pmol/5 min per 2 x 10(6) cells (n = 5) and was not enhanced by exogenous arachidonate. When cells from allergic patients were challenged in the presence of exogenous [1-14C]arachidonic acid, released LTB4 was radiolabeled and the incorporated radioactivity increased with the labeled arachidonate concentration. Labeled LTB4 was never detectable after incubating neutrophils from normal donors with exogenous labeled arachidonate. When neutrophils were incubated with [1-14C]arachidonate for 1 h, the different lipid pools of the two cell populations were labeled but both types of neutrophils produced unlabeled LTB4 in response to ionophore stimulation. The hydrolysis of choline and ethanolamine phospholipids into diacyl-, alkenylacyl- and alkylacyl-species revealed that solely the alkylacyl-subclass of phosphatidylcholine was unlabeled. We conclude (i) that neutrophils from allergic patients stimulated by low ionophore concentration produce more LTB4 than neutrophils from healthy subjects and incorporate exogenous arachidonate, (ii) that endogenous arachidonate converted to LTB4 by the 5-lipoxygenase pathway may provide only from 1-O-alkyl-2-arachidonoyl-glycero-3-phosphocholine.

Adult↗
PubMed1991

Fatty acid composition of the rat pineal gland. Dietary modifications.

When compared to brain, the fatty acid composition of the rat pineal gland revealed that the total proportion of n-6 polyunsaturated fatty acids (PUFA) was 2.3-fold higher, whereas the proportion of n-3 fatty acids was similar. Specifically, 20:4(n-6) and 18:2(n-6) were respectively 1.56- and 11.80-fold higher in the pineal than in the brain, while the proportions of 22:6(n-3) were similar in both tissues. In addition, 18:1(n-9) was found 2.15-fold lower in the pineal. Feeding adult rats with fish oil concentrates induced a significant alteration of the polyunsaturated fatty acid composition of the pineal. There was a reciprocal replacement of the n-6 by the n-3 fatty acids. Conversely, in rats fed a n-3 fatty acid-deficient diet (sunflower oil or coconut oil diet), the pineal gland contained reduced proportions of n-3 fatty acids. We conclude that the pineal gland (i) differs from the brain in containing much higher proportions of 18:2(n-6) and from the other tissues for its high proportions of 22:6(n-3) and (ii) is highly sensitive to the n-3 fatty acid diet in contrast to what is known for the brain. These findings are discussed in the context of melatonin biosynthesis, the major hormone of the pineal gland.

Animals↗
PubMed1991

Dietary polyunsaturated fatty acids modulate fatty acid composition and early activation steps of concanavalin A-stimulated rat thymocytes.

The early biochemical responses to concanavalin A (Con A) of thymocytes from rats fed a saturated (coconut oil), (n-6) (sunflower oil) or (n-3) (fish oil) fatty acid-enriched diet for 3 wk were investigated. Fish oil feeding resulted in greater (n-3) polyunsaturated fatty acid level (PUFA) at the expense of (n-6) PUFA in total and individual thymocyte phospholipids. Such alterations of the fatty acid composition did not affect basal ornithine decarboxylase (ODC), cyclic nucleotide phosphodiesterase (PDE) or gamma-glutamyl transferase activities. However, the fish oil-enriched diet impaired some of the early thymocyte responses to Con A, such as the rapid induction (30 min) of soluble ODC and PDE activities. Synthesis of [3H]20:4(n-6) oxygenated metabolites was not different between the dietary groups; however, the uptake of [3H]20:4(n-6) into phospholipid classes was significantly lower in phosphatidylcholine and greater in phosphatidylethanolamine and phosphatidylinositol after fish oil feeding. Similarly, the Con A-induced remodeling of the [3H]20:4(n-6) esterification in phospholipids differed in sunflower oil- vs. fish oil-fed rats, suggesting a modulation of acyl CoA synthase and/or acyl CoA transferase activities. Thus, the modulation of Con A-induced ODC and PDE stimulation upon in vivo changes of membrane phospholipid fatty acid composition is not related to eicosanoid formation, but rather to the modification of the fatty acid acylation processes, altering phospholipid composition and signal transduction.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1990

Enrichment of platelet phospholipids with eicosapentaenoic acid and docosahexaenoic acid inhibits thromboxane A2/prostaglandin H2 receptor binding and function.

Human platelet lipids were enriched in vitro with different amounts of either docosahexaenoic acid (22:6n-3), eicosapentaenoic acid (20:5n-3) or linoleic acid (18:2n-6). Of the total fatty acid incorporated, between 82 and 95% was associated with the phospholipid (PL) fraction, with the remainder as either neutral lipid or hydroxy fatty acid. Within the PL fraction, the majority (64% of total) of each fatty acid was incorporated into phosphatidylcholine. It was found that platelet aggregation induced by the thromboxane A2/prostaglandin H2 mimetic (15S)-hydroxy-11,9-(epoxymethano)prosta-5Z,13E-dienoic acid (U46619) was inhibited after PL enrichment with 22:6n-3 or 20:5n-3, but not after 18:2n-6 enrichment. The specificity of 22:6n-3 and 20:5n-3 for U46619 activation was demonstrated by the finding that neither fatty acid significantly inhibited thromboxane A2/prostaglandin H2-independent aggregation induced by A23187 or thrombin. Furthermore, enrichment with 22:6n-3 or 20:5n-3 resulted in inhibition of [3H]U46619 specific binding, while enrichment with 18:2n-6 did not affect binding. Scatchard analysis revealed that thromboxane A2/prostaglandin H2 receptor affinity for [3H]U46619 decreased 4.8-fold following 22:6n-3 incorporation. These results demonstrate that platelet phospholipid enrichment with 22:6n-3 or 20:5n-3 results in a selective inhibition of thromboxane A2/prostaglandin H2 receptor function.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Functions and tocopherol content of blood platelets from elderly people after low intake of purified eicosapentaenoic acid.

Elderly people present an increased incidence of atherosclerosis and vascular cerebral damages, associated with blood platelet hyperactivity and a stimulation of arachidonic acid metabolism in vivo. The effects of a low intake of purified eicosapentaenoic acid (EPA) on platelet hyperactivity in old human subjects has been investigated. In a randomized, double blind study, 8 people took during 2 months a daily intake of 100 mg of eicosapentaenoic acid (EPA) given as a triglyceride (1,3-dioctanoyl,2-eicosapentaenoyl-glycerol), and 8 other subjects ingested a placebo. A slight, but significant reduction of platelet-rich plasma aggregation in response to epinephrine and arachidonic acid occurred after EPA intake, as well as a decreased aggregation of washed platelets induced by thrombin, although collagen- and U-46619-induced aggregations were not significantly modified. EPA intake failed to affect arachidonic acid metabolism in thrombin-stimulated platelets or in clotted venous blood. The urinary excretion of thromboxane, 6-keto-PGF1 alpha and their 2,3-dinor-metabolites was also not modified. Similarly, no change in the plasma and platelet lipid fatty acid compositions could be observed. Platelet, but not plasma, alpha- and gamma-tocopherol were enhanced by EPA intake. An increase of platelet vitamin E has been associated with a decrease of aggregation, especially in vitamin E-deficient subjects, like elderly people. Therefore, low intake of EPA might have contributed to inhibit platelet aggregation by increasing cellular vitamin E.

Administration, Oral↗
PubMed1990

Benzodiazepine analogues inhibit arachidonate-induced aggregation and thromboxane synthesis in human platelets.

1. Benzodiazepine analogues inhibit human platelet aggregation induced by arachidonate with an EC50 value of 0.68 microM for PK 11195, the most potent analogue used. 2. There was a highly significant correlation between the inhibition of arachidonate-induced aggregation and the affinity for the peripheral-type of benzodiazepine binding sites. 3. There was no significant correlation between the inhibition of the platelet activating factor (PAF)-induced aggregation and the binding to the peripheral-type of benzodiazepine binding sites. 4. The inhibition of platelet aggregation seems to result from the inhibition of arachidonic acid cyclo-oxygenation, since the synthesis of thromboxane and 12-hydroxy-heptadecatrienoic acid, both cyclo-oxygenase products, was reduced. 5. Our results suggest that peripheral-type of benzodiazepine binding sites on human platelets could be linked to cyclo-oxygenase.

Arachidonic Acid↗
PubMed1989

Effects of dietary n-3 polyunsaturated fatty acids on phospholipid composition and calcium transport in mouse cardiac sarcoplasmic reticulum.

The effects of dietary n-3 and n-6 polyunsaturated fatty acids on the fatty acid composition of phospholipid, Ca++. Mg++ ATPase and Ca++ transport activities of mouse sarcoplasmic reticulum were investigated. Mice were fed a 2 weight percent fat diet containing either 0.5 weight percent ethyl esters of 18:3n-3, 20:5n-3 or 22:6n-3 as a source of n-3 polyunsaturated fatty acid or 0.5 weight percent safflower oil as a source of n-6 polyunsaturated fatty acid for 10 days. Olive oil (2 weight percent) was used as a control diet. Although feeding n-6 polyunsaturated fatty acid induced very little modifications of the phospholipid sarcoplasmic reticulum fatty acid composition, feeding n-3 polyunsaturated fatty acid altered it markedly. Inclusion of 18:3n-3, 20:5n-3 or 22:6n-3 in the diet caused an accumulation of 22:6n-3, which replaced 20:4n-6 and 18:2n-6 in phospholipid sarcoplasmic reticulum. The saturated fatty acids were significantly increased with a concurrent reduction of 18:1n-9. These changes in the fatty acid composition resulted in a decrease in the values of the n-6/n-3 polyunsaturated fatty acid ratio and a decrease in the ratio of 20 carbon to 22 carbon fatty acids esterified in the phospholipid sarcoplasmic reticulum. This was associated with a decrease in Ca++ uptake by n-3 polyunsaturated fatty acid enriched sarcoplasmic reticulum vesicles as compared with n-6 fatty acid and control diet sarcoplasmic reticulum vesicles. However, neither the affinity for Ca++ nor the maximal velocity of ATP hydrolysis activity of Ca++.MG++ATPase were altered by the different diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of small concentrations of eicosapentaenoic acid on platelets.

Increased platelet functions have been associated with enhanced arachidonic acid (AA) metabolism in diabetics and elderly people. We investigated these parameters in both groups after feeding low doses of pure eicosapentaenoic acid (EPA). After such an intake, platelet aggregation induced by various agonists was decreased whereas the oxygenated metabolism of endogenous AA was not substantially altered, and the fatty acid composition of plasma and platelet lipid pools did not change. In the most recent study, the measurement of vitamin E revealed that although its level in plasma was not modified, it was increased in platelets after EPA intake. It is concluded that small amounts of EPA intake do not reduce platelet aggregation in competing with AA metabolism but rather in depressing the peroxide tone of the cell.

Aged↗
PubMed1989

Changes in phospholipid fatty acid composition of mouse cardiac organelles after feeding graded amounts of docosahexaenoate in presence of high levels of linoleate. Effect on cardiac ATPase activities.

Mice were fed diets containing a constant supply of linoleic acid (18:2n-6, LA) as ethyl ester representing 5% by weight of the total fat (5 wt%), in combination with graded amounts of purified docosahexaenoate (22:6n-3, DHA). Cardiac sarcoplasmic reticulum (SR) and mitochondrial phospholipids (PL) from mice fed the diet without DHA contained higher levels of n-6 long chain polyunsaturated fatty acids (PUFA) (22:4n-6 and 22:5n-6) compared to total PL of liver. In the cardiac mitochondrial PL, the level of LA, DHA, the total content of PUFA and the P/S ratio were significantly higher than in SR. A small increase in dietary DHA from 0 to 0.43 wt% induced a 3.6-fold increase in PL DHA content from both cardiac organelles, with a concurrent reduction of n-6 PUFA. The changes in fatty acid PL composition were much more moderate when dietary DHA level was increased to 0.85 and 3.74 wt%. Feeding the lowest amount of DHA resulted in a 6-fold decrease in the value of n-6/n-3 PUFA ratio and a 3.5-fold decrease in the value of 20 carbon chain/22 carbon chain PUFA ratio. DHA was readily depleted from cardiac PL, and only arachidonic acid was retained in the PL from both organelles, after feeding a fat-deficient diet. Despite these drastic modifications in PL fatty acid composition, the maximum velocity (Vm) of SR Ca2+, Mg2+-ATPase was not affected, which indicates that SR cardiac membrane adapts to changes in fatty acid composition to prevent important modifications of its functional properties. However, the Vm of mitochondrial oligomycin-sensitive ATPase was slightly increased in mice fed the lowest amount of DHA. This might be due to an increase in P/S ratio and/or to a modification of cardiolipin fatty acid composition, since this PL is required for optimum function of this enzyme. It is concluded that DHA is strongly taken up by mouse cardiac PL, even in the presence of high dietary LA levels, but its acylation into PL has only little effect on the cardiac ATPase activities.

Animals↗
PubMed1989

Differential effect of SIN-1 on thromboxane and prostacyclin formation in platelets and endothelial cells.

The effect of SIN-1, the active metabolite of molsidomine that inhibits platelet aggregation, was tested upon the oxidation of arachidonic acid in platelets and endothelial cells. The metabolism of arachidonic acid from both exogenous and endogenous sources was investigated by determining the formation of thromboxane and prostacyclin. These prostanoids were measured in platelets and endothelial cells alone or during their interaction, in the absence or presence of SIN-1. The presence of endothelial cells decreased the generation of thromboxane by the platelets, especially from endogenous arachidonate, whereas the platelets tended to increase that of prostacyclin under basal conditions. SIN-1 significantly reduced the production by the platelets of metabolites from endogenous arachidonic acid but did not affect those from exogenous sources. The reduction in metabolism of endogenous arachidonate was more pronounced in the presence of endothelial cells. In contrast, SIN-1 did not alter the production of cyclo-oxygenase metabolites of arachidonic acid in endothelial cells. Thus, the liberation of arachidonic acid, leading to prostanoid synthesis, may be regulated differentially in platelets and endothelial cells: molsidomine might be a potential antithrombogenic drug because it alters specifically the phospholipase activity in the platelets.

Arachidonic Acids↗
PubMed1988

Different metabolic behavior of long-chain n-3 polyunsaturated fatty acids in human platelets.

Whereas numerous studies deal with the effects and metabolism of eicosapentaenoic acid (20:5(n - 3)) in platelets, very few concern docosahexaenoic acid (22:6(n - 3)), although both acids are consumed in equal amounts from most fish fat. The present paper reports the modulation of 22:6(n - 3) oxygenation as well as that of endogenous arachidonic acid (20:4(n - 6)) in 22:6(n - 3)-rich platelets. Like the oxygenation of 20:5(n - 3), the lipoxygenation of 22:6(n - 3) occurred at a low level when incubated alone, but was markedly increased in the presence of 20:4(n - 6), suggesting a similar peroxide tone dependency. 20:5(n - 3) could not replace 20:4(n - 6) in the increasing 22:6(n - 3) lipoxygenation, whereas 22:6(n - 3) shared the potentiating effect of 20:4(n - 6) on both the cyclooxygenation and the lipoxygenation of 20:5(n - 3). On the other hand, 20:5(n - 3), 22:6(n - 3) or 20:5(n - 3) + 22:6(n - 3) enrichment of platelet phospholipids inhibited the formation of cyclooxygenase but not lipoxygenase products from endogenous 20:4(n - 6) in thrombin-stimulated platelets. In doing so, 22:6(n - 3) appeared even more potent than 20:5(n - 3), although it was not liberated after acylation in phospholipids, the opposite of what was observed with 20:5(n - 3). Therefore, it seems that, in contrast to 20:5(n - 3), which may compete with endogenous 20:4(n - 6) at the cyclooxygenase level, 22:6(n - 3) would affect the latter enzyme activity in a different way. We conclude that 20:5(n - 3) and 22:6(n - 3) behave differently and might act synergistically on the inhibition of platelet functions after fish fat intake.

Arachidonic Acids↗
PubMed1988

Inhibition by lipoxygenase products of TXA2-like responses of platelets and vascular smooth muscle. 14-Hydroxy from 22:6n-3 is more potent than 12-HETE.

Lipoxygenase products, which are formed in great amounts in platelets during their activation, have been prepared from arachidonic acid (20:4n-6), the main polyunsaturated fatty acid (PUFA) esterified in platelet phospholipids, and from two major PUFAs of fish fat, eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) acids. These compounds have been synthesized using platelet suspension as enzymic source, purified by high performance liquid chromatography, and their structure were checked by gas chromatography-mass spectrometry. Their effects were investigated in vitro upon human platelet aggregation induced by 11,9-epoxy-methano-analogue of PGH2 (U-46619) and upon thromboxane A2-induced vasoconstriction of rabbit aorta. All hydroxylated fatty acids inhibited U-46619-induced aggregation in a concentration-dependent fashion. Compounds issued from 22:6n-3 were the most potent inhibitors and their IC50 differed significantly from that of 12-hydroxy-eicosatetraenoic acid (12-HETE). Among them, 14-hydroxy-docosahexaenoic acid (14-OH-22:6) was the most effective anti-aggregating molecule (IC50:0.45 microM). 10 microM 12-HETE and 14-OH-22:6 inhibited 60% and 75% of smooth muscle contraction induced by TXA2-like material, respectively. At 1 microM, solely 14-OH-22:6 had an inhibitory effect on adrenaline-, angiotensine- or histamine-induced contraction. Since thromboxane receptors in platelets and vascular smooth muscle cells present strong similarities, it is concluded that hydroxylated fatty acids can antagonize prostanoid action probably by interfering with their receptor sites.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Platelets and aging. II--Plasma lipoproteins and fatty acid profiles.

Lipid composition of both plasma and platelets were investigated in sixteen old (78-94 years) and eight young (25-35 years) subjects. No age-related change was noted in plasma total and HDL cholesterol whereas a slightly increase of triglycerides was observed in the elderly population. Level of apo AI tended to decrease while apo AII decreased significantly in the elderly. These results led to a higher apo AI/apo AII ratio in elder subjects. However, no difference was detected in the level of apo B. In contrast, several modifications appeared in fatty acid composition of plasma lipids. Primarily, monounsaturated fatty acids content was increased while level of linoleic acid (and arachidonic acid in phospholipids) decreased in each class of plasma lipids of elderly subjects. In platelets from the elderly, we found an enhancement of monounsaturated fatty acids in phosphatidyl-inositol (PI), -ethanolamine (PE) and -choline (PC). The decrease of linoleic acid was detected in PC while the reduction of AA was noted in PE. These results indicate that modifications of fatty acid composition in both plasma and platelet lipids appeared with aging. They might be linked to the enhanced platelet activation in vivo observed in elderly people.

Adult↗
PubMed1988

Platelets and aging. I--Aggregation, arachidonate metabolism and antioxidant status.

Platelet functions were investigated in sixteen old (78-94 years) and eight young (25-35 years) subjects. Whole blood platelet aggregation induced by collagen was higher in the elderly. Similarly, aggregation of platelet rich plasma and plasma-free platelets induced by various agents was increased but the collagen-induced release of ATP was reduced. In agreement with the enhanced platelet aggregability, the increase of thromboxane formation (under thrombin stimulation) was also noted in platelets from elderly people. To further assess platelet and vascular function in vivo, we measured the excretion of urinary TXB2, 2,3-dinor TXB2, 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha. The four metabolites were all increased in the elder population. In addition, a significant reduction of platelet vitamin E was observed in the elderly people, although the plasma content was normal. These results indicate numerous modifications of platelet behaviour with aging. They include the increased platelet susceptibility to aggregation, and the depletion of ATP granule content, which could reflect an activation in vivo in agreement with the enhanced urinary excretion of thromboxane and prostacyclin metabolites. We hypothesize that platelet hyperactivity associated with the enhanced oxygenated metabolism of arachidonic acid could be linked to vitamin E depletion. These changes may reveal a prethrombotic state in the elderly population.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1988

Vitamin E fails to alter the aggregation and the oxygenated metabolism of arachidonic acid in normal human platelets.

Using low doses of vitamin E, either in vitro or in vivo, we have succeeded in almost doubling plasma and platelet alpha-tocopherol in healthy humans. Despite such an enrichment, platelet aggregation induced by collagen and thromboxane A2 minetic U46619 was not much affected, although that induced by exogenous arachidonic acid was significantly decreased. Similarly, the oxygenation of exogenous arachidonic acid was not modified. When incubated with thrombin some variations in the formation of endogenous cyclooxygenase and lipoxygenase products could be observed, although rarely significantly. The tendency was a decrease after in vivo enrichment and an increase when enrichment occurred in vivo. Serum oxygenated metabolites of arachidonic acid as well as urinary metabolites of thromboxane and prostacyclin were also not affected after vitamin E supplementation. Since the lipoxygenation of eicosapentaenoic acid was very strongly peroxide-dependent, the effect of alpha-tocopherol enrichment was tested and the 12-hydroperoxide derivative of arachidonic acid was used as a physiological peroxide. No modification could be observed, confirming that vitamin E does not alter the specific peroxidation of polyunsaturated fatty acids in normal platelets. We conclude that vitamin E supplementation neither affects arachidonic acid-dependent aggregation nor the oxygenated metabolism of arachidonic acid in normal human platelets.

Adult↗
PubMed1986

In vitro incorporation and metabolism of icosapentaenoic and docosahexaenoic acids in human platelets--effect on aggregation.

Washed human platelets were pre-loaded with icosapentaenoic acid (EPA), docosahexaenoic acid (DHA) or EPA + DHA and tested for their aggregation response in comparison with control platelets. In fatty acid-rich platelets, an inhibition of the aggregation could be observed when induced by thrombin, collagen or U-46619. The strongest inhibition was observed with DHA-rich platelets and it was reduced when DHA was incorporated in the presence of EPA. Study of fatty acid distribution in cell lipids after loading showed that around 90% of EPA or DHA taken up was acylated into phospholipids and a very small amount (less than 2%) remained in their free and hydroxylated forms. DHA was more efficiently acylated into phosphatidylethanolamine (PE) than into phosphatidylinositol (PI) in contrast to what observed with EPA, and both acids were preferentially incorporated into phosphatidylcholine (PC). EPA inhibited total incorporation of DHA and increased its relative acylation into PE at the expense of PC. In contrast, DHA did not affect the acylation of EPA. Upon stimulation with thrombin, EPA was liberated from phospholipids and oxygenated (as judged by the formation of its monohydroxy derivative) whereas DHA was much less metabolized, although consistently transferred into PE. It is concluded that EPA and DHA might affect platelet aggregation via different mechanisms when pre-loaded in phospholipids. Whereas EPA is known to alter thromboxane A2 metabolism from endogenous arachidonic acid, by competing with it, DHA might act directly at the membrane level for inhibiting aggregation.

Biological Transport↗