Abstract
Essential fatty acid deficient (EFA deficient) hairless mice were used to test the ability of topical agents to reduce the high epidermal DNA synthesis and acanthosis present in EFA deficiency. An established therapeutic agent known to be effective in psoriasis (betamethasone 17-valerate) significantly reduced the epidermal DNA synthesis, mitotic count and epidermal cell thickness. Linoleic acid reduced DNA synthesis and returned epidermal histology towards that of normal skin. Prostaglandin E2 analogue (15 (S)-15-methyl PGE2 methyl ester) reduced epidermal DNA synthesis both in treated and distant skin sites. Prostaglandin E2 was less effective than the analogue but slightly reduced epidermal DNA synthesis and thickness. Prostaglandin F2alpha had no obvious effect on the epidermis. Chlorambucil reduced epidermal DNA synthesis and thickness. Vitamin A acid increased DNA synthesis and epidermal cell thickness but reduced the hyperkeratosis of EFA deficiency. A rapid epidermal cell transit was found in EFA deficient mice, approximately three times faster than in normal mouse epidermis.
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