2001 Volume 47 Issue 1 Pages 69-77
Arachidonic acid (20:4 n-6) and its metabolic products, such as prosta-glandins and leukotrienes, have been known to be associated with skin inflammatory reac-tions. However, the mechanism of the competitive incorporation of 20:4 n-6 into ke-ratinocytes among polyunsaturated fatty acids (PUFAs) remains uncertain. To investigate the relationship between the molecular structure of PUFAs and the rate of incorporation of PUFAs into cells, a fetal rat skin keratinocyte (FRSK) cell line was used. The cells were incu-bated for 24 h with any two of the following arachidonic acid analogs: mead acid (20:3 n-9), dihomo-γ-linolenic acid (20:3 n-6), 11, 14, 17-cis-eicosatrienoic acid (20:3 n-3), arachi-donic acid (20:4 n-6), eicosapentaenoic acid (20:5 n-3) and 5, 8, 11, 14-cis-nonadecate-traenoic acid (19:4 n-5), at the ratio of 1:0, 0.5:0.5, or 0:1; and their incorporation into lipid was measured by capillary gas-liquid chromatography. The experiments indicated that 20:3 n-6 was preferentially incorporated into phospholipids of FRSK rather than 20:3 n-9 or 20:3 n-3, and 19:4 n-5 as well as 20:4 n-6 was preferentially incorporated into total cel-lular lipid and phospholipids rather than 20:3 n-9 or 20:5 n-3. When two PUFAs were added simultaneously to the medium, 19:4 n-5 most effectively reduced the competitive in-corporation of 20:4 n-6 into phospholipids. These results suggest that keratinocytes dis-criminate 20:4 n-6 from other arachidonic acid analogs by its double bond positions from the carboxyl group.
