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The relationship between cyclic adenosine 3', 5' - monophosphate and biochemical events in rat skin after the induction of epidermal hyperplasia using hexadecane.

Abstract
Sequential changes in skin metabolism have been studied in a model system of epidermal hyperplasia and hyperkeratinization induced by the application of n-hexadecane to shaved rat skin. The epidermal accumulation of glycogen typical of the hyperplastic response has been correlated with an increase in glycogenesis and a decrease in glycogenolysis. DNA synthesis was increased by 6 h after the start of hexadecane treatment and reached a maximum after one day. The concentration of skin cyclic AMP fell immediately after hexadecane application and subsequently rose to give a prolonged increase. Use of the combined topical application of hexadecane and the anti-inflammatory drugs triamcinolone acetonide, hydrocortisone and indomethacin showed that the hexadecane-induced changes in DNA synthesis and glycogen metabolism were linked to the initial fall in cyclic AMP concentration. The significance of the biphasic change in cyclic AMP levels is discussed as a possible system of control for the development and maintenance of hyperplasia.
AuthorsR F Peters, A M White
JournalThe British journal of dermatology (Br J Dermatol) Vol. 98 Issue 3 Pg. 301-14 (Mar 1978) ISSN: 0007-0963 [Print] England
PMID205235 (Publication Type: Journal Article)
Chemical References
  • Alkanes
  • Anti-Inflammatory Agents
  • Glycogen
  • DNA
  • Cyclic AMP
  • Glycogen Synthase
  • Triamcinolone Acetonide
  • n-hexadecane
  • Hydrocortisone
  • Indomethacin
Topics
  • Administration, Topical
  • Alkanes
  • Animals
  • Anti-Inflammatory Agents (pharmacology)
  • Cyclic AMP (metabolism)
  • DNA (biosynthesis)
  • Epidermis (metabolism, pathology)
  • Glycogen (metabolism)
  • Glycogen Synthase (metabolism)
  • Hydrocortisone
  • Hyperplasia (chemically induced, metabolism)
  • In Vitro Techniques
  • Indomethacin (pharmacology)
  • Male
  • Rats
  • Skin (drug effects, enzymology, metabolism)
  • Triamcinolone Acetonide (pharmacology)

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