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Investigation of functions of essential fatty acids in the skin
Authors:C. PROTTEY
Affiliation:Environmental Safery Division, Unilever Research Laboratory, Colworth House, Sharnbrook, Bedford MK44 iLQ
Abstract:Essential fatty acid-deficient rats develop scaly skin that has impaired barrier properties and lowered concentrations of linoleic and arachidonic acids in phospholipids. Topical linoleic acid restores impaired barrier function to normal (within 5 days) and increases the amount of linoleic acid in skin lecithin, but has no effect on the low levels of arachidonic acid in this phospholipid, or on skin scaliness, during this time. Topical butyl PGE1 or butyl PGE2 for 1 week have no effect on scaliness, impaired barrier function or lipids. Also, the effect of linoleic acid on barrier function is seen even when prostaglandin synthesis has been inhibited by repeated administration of indomethacin. Intraperitoneal linoleic acid also repairs barrier function but has no simultaneous effect on scaliness; and arachidonic acid, similarly administered, rapidly heals skin scaliness, without simultaneously repairing barrier function. Hypophysectomized rats, which grossly resemble essential fatty acid-deficient rats (their skin is scaly), exhibit virtually normal skin fatty acids, and skin permeability is normal, but such animals do not synthesize prostaglandins. These date indicat that of the 2 major essential fatty acids of rat skin, linoleic and arachidonic acids, athe former is found esterified to phospholipids of epidermal membrancs and is also important in the maintenance of the cutanecous barrier to water loss, whereas the latter, although also found in phospholipids, plays no part in barrier function. rather, it is important as a precursor of prostaglandins, which are thought to be involved in the regulation of normal cell division and differantiation of the epidermis, and, consequently, the control of skin scaliness. Hypophysectomized rats and essential fatty acid-deficient rats are similar as neither can synthesize adequate prostagladins, the former probably because the multi-enzyme complex of prostaglandin synthetase in faulty, the latter due ot ethe absence of essential fatty acid precursors.
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