On May 10, 3:41 am, monty1...@lycos.com wrote:

It seems that rather the shorter PUFAs such as linoleic acid (LA,
Omega-6) or MUFAs such as oleic acid (Omega-9 precursor to Mead acid)
play a role in the barrier function:

Arch Dermatol Res. 1999 Jan;291(1):47-53.

Fatty acid uptake by cultured human keratinocytes grown in medium
deficient in or supplemented with essential fatty acids.

Schürer NY, Rippke F, Vogelsang K, Schliep V, Ruzicka T.
Department of Dermatology, University of Düsseldorf, Germany.

Epidermal linoleic acid, i.e. essential fatty acid (EFA), is essential
for cutaneous barrier function. Cultured human keratinocytes,
routinely used for studies of lipid metabolism, are grown in a
keratinocyte serum-free medium (KSFM), under conditions that reveal
EFA-deficient cells. Here, fatty acid (FA) uptake was analysed in
human adult keratinocytes grown either under EFA-deficient conditions
[KSFM supplemented with 10% FCS (A) or 1% UltroserG (B)] or EFA-
supplemented conditions [KSFM supplemented with a devised FA cocktail
(C) or evening primrose oil (D)]. The FA composition of the total
cellular lipid and major lipid fractions was analysed by gas
chromatography. Cells grown with supplements A or B balanced their EFA-
deficient state primarily with oleic acid. Cells grown with
supplements C or D normalized to the epidermal FA composition in vivo
with raised linoleic and lower oleic acid contents. When cells were
grown longer than 48 h with supplements C or D decreased cell growth
was observed. FA uptake was curvilinear with preference for linoleic
over oleic acid under all culture conditions. The uptake of linoleic
acid by cells cultured with supplement B was twice the uptake of those
cultured with supplement A, while the uptake of oleic acid was similar
under both culture conditions. Oleic acid uptake of cells cultured
with supplement C or D was lower. These results show that the uptake
of linoleic, but not that of oleic acid, is influenced by the
extracellular FA composition, and that EFA-supplemented keratinocytes
compared to EFA-deficient cells might serve as an in vitro model for
the study of EFA metabolism.
PMID: 10025727

J Invest Dermatol. 1980 Apr;74(4):230-3.

The permeability barrier in essential fatty acid deficiency: evidence
for a direct role for linoleic acid in barrier function.

Elias PM, Brown BE, Ziboh VA.

Essential fatty acid (EFA) deficient rodents demonstrate abnormal
epidermal permeability barrier function and differentiation, defects
which can be corrected by either topical or systemic administration of
linoleic acid. Since linoleic acid is a precursor of prostaglandins,
correction of the defect in barrier function may either reflect a
prostaglandin-mediated return toward normal epidermal differentiation,
or, instead, a direct effect of linoleic acid. To test these
possibilities severely EFA-deficient mice were pretreated daily with
indomethacin and/or 5,8,11,14-eicosatetrayeonic acid, and then placed
on normal (lineolic acid-supplemented) diets. Endogenous formation of
prostaglandin E2 was determined by thin-layer chromatography after
transformation into prostaglandin B2 with ethanolic-hydrochloric acid.
Animals treated with both indomethacin and TYA DEMONSTRATED
SUBSTANTIAL REDUCTIONS IN PROSTAGLANDIN E2 levels in liver and skin.
Animals replenished with linoleic acid invariably demonstrated a rapid
return of barrier function toward normal whether or not they were
blockaded, while nonreplenished animals, with or without inhibition of
prostaglandin biosynthesis, demonstrated continued deterioration in
barrier function. In other experiments, topically applied linoleic
acid rapidly reversed the defect in barrier function at the sites of
application prior to systemic correction of the EFA deficient state.
These results suggest that: (1) defective cutaneous barrier function
in EFA deficiency can be corrected locally without prior systemic
reversal of the deficiency state; and (2) that linoleic acid may play
a direct role in the epidermal permeability barrier independent of its
role in prostaglandin metabolism.
PMID: 7373078

J Clin Invest. 1994 Jul;94(1):89-96.

Pseudo-acylceramide with linoleic acid produces selective recovery of
diminished cutaneous barrier function in essential fatty acid-
deficient rats and has an inhibitory effect on epidermal hyperplasia.

Imokawa G, Yada Y, Higuchi K, Okuda M, Ohashi Y, Kawamata A.
Tochigi Research Laboratories, Kao Corporation, Japan.

Pseudo-acylceramides with different acyl properties were investigated
for their capacity to restore diminished barrier function in essential
fatty acid-deficient rats. Daily topical applications of synthetic
pseudo-acylceramides containing ester-linked linoleic acid caused a
dose-dependent, significant reduction of transepidermal water loss
(TEWL). Both other pseudo-acylceramides with ester-linked oleic acid
or saturated alkyl chains and ordinary ceramides exhibited a poor
effect on recovery of TEWL. Furthermore, pseudoceramide containing
ether-linked linoleic acid, which is biologically inactive in terms of
degradation by hydrolytic enzymes, also induced a significant and
similar increase in the barrier function. This restoration of barrier
function by pseudo-acylceramides with linoleic acid was accompanied by
suppressed DNA synthesis in the EFAD rat epidermis. In UVB-irradiated
guinea pig skin, topical applications of the pseudo-acylceramides with
linoleic acid immediately after the exposure significantly reduced
epidermal hyperplasia, secondary to markedly diminished barrier
disruption, whereas linoleic acid itself did not. A comparison of both
the anti-hyperplasia and the barrier recovery effects in the series of
pseudo-ceramide derivatives examined revealed that the suppressive
effect on the induced epidermal hyperplasia was paralleled by the
recovery of the barrier defect in EFAD rats. These findings directly
suggest that acylceramide with an ester-linked linoleic acid has an
essential role in the epidermal permeability barrier.
PMID: 8040295

Br J Dermatol. 1976 Jan;94(1):13-21.

The repair of impaired epidermal barrier function in rats by the
cutaneous application of linoleic acid.

Prottey C, Hartop PJ, Black JG, McCormack JI.

Epidermal barrier function in rats was experimentally impaired by two
separate means, namely, by rendering the animals deficient in
essential fatty acids and by evoking a primary cutaneous irritant
response by treating with a solution of sodium laurate. Impaired
barrier function was manifested by a greatly increased rate of
transepidermal water loss. Application to the skin of sunflower seed
oil, which is rich in linoleic acid, rapidly restored to normal the
abnormally high rates of transepidermal water loss in both
experimental cases, and it was shown with the essential fatty acid-
deficient rats that there was a concomitant incorporation of linoleic
acid of the sunflower seed oil into epidermal lipids. Cutaneous
application of olive oil, which is low in linoleic acid but rich in
the non-essential oleic acid, did not influence epidermal barrier
function. A close relationship of barrier function and essential fatty
acids is indicated.
PMID: 1252336