Precursor- and pool-dependent differential effects of ethanol on human platelet prostanoid synthesis

Microsomal Δ9, Δ6 and Δ5 desaturase activities and liver membrane fatty acid profiles in alcohol‐fed rats

“…Ethanol-induced increases in the synthesis of these compounds may also alter the fatty acid composition of the membrane phospholipids. Enhanced synthesis of prostaglandin E, by ethanol has been reported (Segarnick et al, 1985) and has been implicated in some of the changes in fatty acid composition of mitochondrial phospholipids produced by ethanol (Horrobin, 1980). This may explain our microsomal phospholipid findings without change in A6 desaturase activity.…”

Effect of ethanol on platelet phospholipase A2

“…There is considerable evidence that ethanol exerts an inhibitory effect on platelet aggregation (1)(2)(3)(4)(5)(6)(7)(8), and it is possible that this could contribute to its attenuating effect in cardiovascular disease (reviewed in ref. 9).…”

“…9). A number of studies have shown that ethanol inhibits the synthesis of prostanoids including thromboxane A2, which is involved in the aggregation process (1)(2)(3)(4)(5)(6)(7). These findings would imply that ethanol reduces the level of arachidonic acid release Indeed addition of exogenous arachidonic acid is known to alleviate the effect of ethanol (ag., see ref.…”

Essential Fatty Acids, Prostaglandins, and Nonsteroidal Antiinflammatory Agents: Physiological and Behavioral Interactions

“…In the context of the EFA-ethanol interactions described in this review, Segarnick et al 3 have provided evidence from studies with human platelets which suggest that ethanol affects PG synthesis only from the free EFA pool, and not from the membrane-esterified pool. If a similar situation existed in brain, this might explain how small doses of exogenous EFAs could so potently alter responses to ethanol.…”

“…Much of the thinking in this area has been based on reports that ethanol alters EFA absorption, metabolism, and conversion to PGs in a variety of tissues and species. [1][2][3][4] In 1980, Horrobin and Manku5 proposed a unifying hypothesis regarding ethanol's mechanism of action which described the role of EFAs and PGs as central mediators of ethanol's behavioral effects. To briefly summarize, Horrobin's hypothesis was based on a series of reports indicating that physiologically relevant doses of ethanol stimulate the conversion of EFAs to P G S .…”