AbstractEthanol, over the concentration range 33 to 300 mg/100 ml (7.2-65.2 x 10-3 M) caused a dose dependent and highly significant enhancement of conversion of 14C-dihomogammalinolenic acid (DGLA) to prostaglandin (PG) El and to thromboxane (Tx) B1 by human platelets. Ethanol had no significant effect on conversion of 14C-arachidonic acid to PGE2 and TxB2. This concentration range is the one involved in human alcoholic intoxication. The effect could be related to enhanced transport of DGLA to the active site of the cyclo- oxygenase enzyme complex, to a modification of the enzyme complex which changes the way it metabolizes DGLA but not arachidonic acid or to two different enzymes. Whatever the mechanism it seems that it is possible to regulate selectively the formation of 1 and 2 series PGs probably at the cyclo-oxygenase level. The physiological and clinical implications of this are discussed.
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