Incorporation of alpha-linolenic acid and linoleic acid into human respiratory epithelial cell lines

Citation
Dl. Bryan et al., Incorporation of alpha-linolenic acid and linoleic acid into human respiratory epithelial cell lines, LIPIDS, 36(7), 2001, pp. 713-717
Citations number
19
Categorie Soggetti
Agricultural Chemistry","Biochemistry & Biophysics
Journal title
LIPIDS
ISSN journal
00244201 → ACNP
Volume
36
Issue
7
Year of publication
2001
Pages
713 - 717
Database
ISI
SICI code
0024-4201(200107)36:7<713:IOAAAL>2.0.ZU;2-V
Abstract
Animal and human studies designed to examine the effects of alpha -linoleni c acid (ALA) and linoleic acid (LA) supplementation on the fatty acid compo sition of plasma and tissues have demonstrated a marked difference in incor poration into phospholipids of these 18-carbon precursors of the long-chain polyunsaturates. Whereas tissue phospholipid levels are linearly related t o dietary ALA and LA, the levels of tissue LA can be 10-fold higher than ti ssue ALA even when dietary levels are equivalent. There is some dispute whe ther this disparity is due to ALA being more rapidly metabolized to its pro ducts or substantially oxidized by the liver, or whether LA but not ALA is readily incorporated into cellular phospholipids. We examined the level of incorporation of polyunsaturated fatty acids into human respiratory epithel ial cell lines (A549, 16HBE) by determining the dose-dependent incorporatio n of ALA and LA as free fatty acid (5-150 mug FFA/mL). Cell membrane phosph olipid ALA and LA were both increased up to similar to 20-30% total fatty a cids, with a concomitant decrease predominantly in monounsaturated membrane fatty acids, before significant toxicity was observed (50 mug/mL). Our dat a support the concept that rather than any inherent inability by human cell s to incorporate ALA into membrane phospholipids, the lack of ALA content i n human and animal tissues in vivo is due to the rapid metabolism or oxidat ion of this fatty acid in the liver.