Abstract
The arachidonic acid released from cellular phospholipids of specifically stimulated platelets and leukocytes is oxygenated enzymatically by two major pathways1–5. A complex cyclo-oxygenase converts some of the free arachidonic acid to labile endoperoxides that are transformed to prostaglandins, thromboxanes and prostacyclin (PGI2). Lipoxygenases convert part of the arachidonic acid to unstable hydroperoxy-eicosatetraenoic acids (OOHETEs) that are transformed to monohydroxy-eicosatetraenoic acids (HETEs), oligohydroxy-eicosatetraenoic or -eicosatrienoic acids such as di-HETEs and tri-HETEs, and, in some instances, more complex humoral mediators, including slow-reacting substances5–9. Both the nature of the HETEs and the ratio of the HETEs to the cyclo-oxygenase products are specific characteristics of each type of cell2,5. In human neutrophils, the sum of the lipoxygenase products 5-HETE, 11-HETE and 5,12-di-HETE substantially exceeds the total amount of PGE2 and other cyclo-oxygenase metabolites that are generated concurrently3,4, and the endogenous lipoxygenase products regulate neutrophil function. The present data indicate that vitamin E (α-tocopherol) bidirectionally modulates the activity of the lipoxygenase pathway of human neutrophils in vitro. Normal plasma concentrations of α-tocopherol enhance the lipoxygenation of arachidonic acid, whereas higher concentrations of α-tocopherol exert a suppressive effect that is consistent with its role as a hydroperoxide scavenger.
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Goetzl, E. Vitamin E modulates the lipoxygenation of arachidonic acid in leukocytes. Nature 288, 183–185 (1980). https://doi.org/10.1038/288183a0
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DOI: https://doi.org/10.1038/288183a0
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