13hpotre(r)

13(S)-HpOTrE(γ) is a monohydroxy PUFA produced by the action of soybean lipoxygenase-1 (LO-1) on γ-linolenic acid. Further action of soybean LO-1 converts 13(S)-HpOTrE(γ) to all four isomers of 6,13-DiHOTrE. At concentrations greater than 100 μM, 13(S)-HpOTrE(γ) inhibits the activity of soybean LO-1.

13(S)-HpOTrE is a monohydroperoxy polyunsaturated fatty acid produced in soybeans by the action of soybean LO-2 on esterified α-linolenic acid.[1] Incubation of soybean seedling biomembranes with soybean LO-2 catalyzes the formation of both 9- and 13-HpOTrE in a molar ratio of 10:1.1 In plants, 13(S)-HpOTrE can be metabolized by the hydroperoxide lyase pathway producing aldehyde and oxoacid fragments, or by the hydroperoxide dehydratase pathway producing jasmonic acid.[2],[3],[4] Treatment of tomato leaves with 13-HpOTrE causes induction of proteinase inhibitors, simulating the normal response to wounding.5 This data suggests that in plants 13(S)-HpOTrE may participate in a lipid-based signalling system initiated by insect and pathogen attack.

13(R)-HODE cholesteryl ester was originally extracted from atherosclerotic lesions. It remains uncertain whether the oxidized fatty acid portion of the molecule results from enzymatic lipoxygenation or from random lipid peroxidation. 13(R)-HODE cholesteryl ester can be used as a standard for analysis of chiral HODE cholesteryl esters.

Fluprostenol isopropyl ester, a potent agonist of the F-series prostaglandin receptor, serves as a prodrug utilized clinically as an ocular hypotensive agent for glaucoma treatment. An impurity, 13(R),14(R)-epoxy fluprostenol isopropyl ester, arises during its production, existing as a chiral enantiomer of the epoxide. The pharmacological properties of this specific enantiomer have yet to be thoroughly investigated.

13(R)-HODE is the opposite enantiomer of the 13(S)-HODE produced when linoleic acid is incubated with soybean lipoxygenase. The presence of 13(R)-HODE in the supernatants and membranes of cultured bovine endothelial cells has been attributed to COX metabolism. 13(R)-HODE is a weak (IC50 = 2.7 μM) inhibitor of U-46619-induced platelet aggregation.