Effect of ethanol on platelet phospholipase A₂

Abstract

Platelet aggregation is known to be inhibited by ethanol, and this has been suggested to be one of the attenuating effects of ethanol in cardiovascular disease. Recent studies have implicated an inhibition of phospholipase A2 induced arachidonic acid release, since the production of prostanoids that are formed from arachidonic acid and are involved in the aggregation process has been shown to be diminished by ethanol. Phospholipase A2 is found in platelets in both a cytosolic form, from where it may translocate to the plasma membrane to release arachidonic acid, and in a secretory form which is released extracellularly upon activation. In the present study, the effect of ethanol on the secretion of phospholipase A2 and on its activity was determined. It was found that ethanol inhibited phospholipase A2 secretion but not its activity. By contrast, the activity of the cytosolic form of phospholipase A2 was inhibited by ethanol.

Antiatherogenic potential of red wine: clinician update

“…Resveratrol and other polyphenolic compounds decrease platelet aggregation, possibly by interfering with prostaglandin synthesis and ADP-mediated aggregation (28,72,112). Similarly, ethanol inhibits in vitro platelet secretion and aggregation, in part by inhibiting phospholipase A 2 secretion and activity (74,95). In vivo, platelet aggregation was inhibited after healthy human volunteers consumed purple grape juice, suggesting grapederived flavonoids and not just ethanol, may contribute to the apparent antithrombotic effect of red wine (36) (see Fig.…”

Alcohol consumption and risk of coronary heart disease among individuals with type 2 diabetes

“…In free-living populations, alcohol may also be positively associated with plasma levels of the thrombolytic tissue type plasminogen activator, independent of HDL-C levels [20]. Additionally, platelet aggregation is inhibited by ethanol [21,22]. This may be particularly important in type 2 diabetics who are prone to increased platelet aggregability.…”

Diet and haemostatic processes

“…Acetaldehyde, one of the products of alcohol metabolism, could react with coagulation proteins to alter their function (Basista et al 1994) or form adducts with platelets which may interfere with their activation and aggregation (Spertini et al 1992). Another possibility is that ethanol inhibits secretion of phospholipase A2 (EC 3.1.1.4) with resultant suppressed arachidonic acid release from platelet membranes, and decreased prostanoid formation and aggregation responses (Stubbs & Rubin, 1992). The differences in acute (postprandial) and long term effects suggest that ethanol and its metabolic products may have different and even opposing effects on haemostatic variables.…”