Elsevier

The Lancet

Volume 355, Issue 9211, 8 April 2000, Page 1273
The Lancet

Correspondence
Hypertension and ascorbic acid

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    This implies that PUFAs themselves may not be able to bring about all their benefits and possibly, they need to be metabolized to their beneficial products such as PGE1, PGI2, PGI3, lipoxins, resolvins, and protectins and enhance the formation of endothelial nitric oxide, which have antiatheroslcerotic, antiplatelet, and vasodilator actions that account for their protective action against CAD and HF. It is known that many cofactors are needed for the conversion of the administered/endogenous PUFAs to their beneficial metabolites, some of which include minerals, vitamins, and trace elements [9,10,13] and hence, their availability in adequate amounts is equally essential to derive their benefits. Additionally, conversion of dietary EFAs (linoleic acid [LA] and α-linolenic acid [ALA]) to their respective long-chain metabolites AA and EPA, and DHA, respectively, need adequate activities of enzymes Δ6 and Δ5 desaturases and elongases, and for the formation of their respective PGs, leukotrienes, thromboxanes, lipoxins, resolvins, and protectins physiologically active COXs and 5-, 12-, and 15-lipoxygenases are essential (Fig. 1).

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