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January 1973

Defects and Deficiency of Adenyl Cyclase in Psoriatic Skin

Author Affiliations

Miami, Fla

From the departments of dermatology and biochemistry, University of Miami, and the Dermatology Service, Veterans Administration Hospital, Miami, Fla. Dr. Mandy is now with the US Air Force Medical Center, Keesler Air Force Base, Biloxi, Miss.

Arch Dermatol. 1973;107(1):47-53. doi:10.1001/archderm.1973.01620160019003

A deficiency of adenyl cyclase in psoriatic skin has been demonstrated in skin slices incubated with tritiated adenine, and in broken-cell preparations (650-g pellets) incubated with adenine triphosphate tagged with phosphorus 32. Tritiated cyclic 3′, 5′-adenine monophosphate (cAMP) formed from tritiated adenine in psoriatic plaques is significantly lower than in adjacent uninvolved skin.

The 650-g pellet prepared from psoriatic plaques has less adenyl cyclase activity than preparations of uninvolved skin. Furthermore, the enzyme in uninvolved skin of patients and in skin of control subjects responds to the stimulation of sodium fluoride and epinephrine, but the enzyme in psoriatic plaques is unresponsive to NaF, and less responsive to epinephrine. In view of the importance of cAMP in regulating cellular activities, the deficiency and abnormal behaviors of adenyl cyclase in psoriatic skin deserves attention. The relevance of observed abnormalities in adenyl cyclase to the pathogenesis of psoriasis remains to be ascertained.