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UV light may induce hypertrichosis through production of PGE2
Medical Hypotheses
Volume 68, Issue 4, 2007, Pages 917-918
M.R. Namazi
Dermatology Department, Shiraz University of Medical Sciences, Shiraz, Iran
Sunlight has been known to have the tendency to induce hypertrichosis – an effect potentiated by some agents such as psoralen and benoxaprofene [1]. The mechanism underlying this effect has not, however, been explained so far. Below, a mechanism is suggested to account for this interesting phenomenon:
UV irradiation is a potent inducer of cyclooxygenase (COX)2 enzyme and produces high levels of PGE2 in the skin [2]. PGE2 is known to stimulate hair growth. Prostaglandins have been reported to stimulate eyelash growth in patients using them in eye preparations for glaucoma and body and scalp hair growth when used topically in various animal models. Interestingly, it has even been proposed that a large part of minoxidil’s therapeutic efficacy against hair loss could be attributed to its activation of prostaglandin H synthase (PGHS)-1 which produces high levels of PGE2 [3].
How PGE2 induces hair growth? PGE2 is known to increase intracellular cAMP levels [4]. Glucose-6-phosphate dehydrogenase (G6PD) activity is then stimulated by cAMP, which increases during the anagen cycle [5]. It should be noted that the inhibitory effect of dehydrotestosterone and dehydroepiandrosterone on hair growth has been attributed to their inhibitory effects on adenyl cylase and G6PD, respectively [5].
Therefore, given that UV irradiation produces PGE2 as the result of its activation of (COX)2, and that PGE2 stimulates hair growth, it could be reasoned that UV light may produce hypertrichosis through production of PGE2.
References
[1] R.P.R. Dawber, D. de Beker and F. Wojnarowska, Disorders of hair (6th ed.). In: R.H. Champion, J.L. Burton and F.J.G. Ebling, Editors, Rook’s textbook of dermatology vol. 3, Blackwell Scientific Publications, Oxford (1998), p. 2894.
[2] I.F. Orengo, J. Gerguis, R. Philips, A. Guevava, A.T. Lewis and H.S. Black, Celecoxib, a cyclooxygenase 2 inhibitor as a potential chemopreventive to UV-induced skin cancer, Arch Dermatol 138 (2002), pp. 751–755. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (55)
[3] R. Wolf, H. Matz, M. Zalish, A. Pollack and E. Orion, Prostaglandin analogs for hair growth: great expectations, Dermatol Online J 9 (2003) (3), p. 7. View Record in Scopus | Cited By in Scopus (6)
[4] M.R. Namazi, The beneficial and detrimental effects of linoleic acid on autoimmune disorders, Autoimmunity 37 (2004) (1), pp. 73–75. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (2)
[5] W.F. Bergfeld, Androgenetic alopecia:next term an autosomal dominant disorder, Am J Med 98 (1995) (Suppl. 1A), pp. 95S–98S.
Medical Hypotheses
Volume 68, Issue 4, 2007, Pages 917-918
M.R. Namazi
Dermatology Department, Shiraz University of Medical Sciences, Shiraz, Iran
Sunlight has been known to have the tendency to induce hypertrichosis – an effect potentiated by some agents such as psoralen and benoxaprofene [1]. The mechanism underlying this effect has not, however, been explained so far. Below, a mechanism is suggested to account for this interesting phenomenon:
UV irradiation is a potent inducer of cyclooxygenase (COX)2 enzyme and produces high levels of PGE2 in the skin [2]. PGE2 is known to stimulate hair growth. Prostaglandins have been reported to stimulate eyelash growth in patients using them in eye preparations for glaucoma and body and scalp hair growth when used topically in various animal models. Interestingly, it has even been proposed that a large part of minoxidil’s therapeutic efficacy against hair loss could be attributed to its activation of prostaglandin H synthase (PGHS)-1 which produces high levels of PGE2 [3].
How PGE2 induces hair growth? PGE2 is known to increase intracellular cAMP levels [4]. Glucose-6-phosphate dehydrogenase (G6PD) activity is then stimulated by cAMP, which increases during the anagen cycle [5]. It should be noted that the inhibitory effect of dehydrotestosterone and dehydroepiandrosterone on hair growth has been attributed to their inhibitory effects on adenyl cylase and G6PD, respectively [5].
Therefore, given that UV irradiation produces PGE2 as the result of its activation of (COX)2, and that PGE2 stimulates hair growth, it could be reasoned that UV light may produce hypertrichosis through production of PGE2.
References
[1] R.P.R. Dawber, D. de Beker and F. Wojnarowska, Disorders of hair (6th ed.). In: R.H. Champion, J.L. Burton and F.J.G. Ebling, Editors, Rook’s textbook of dermatology vol. 3, Blackwell Scientific Publications, Oxford (1998), p. 2894.
[2] I.F. Orengo, J. Gerguis, R. Philips, A. Guevava, A.T. Lewis and H.S. Black, Celecoxib, a cyclooxygenase 2 inhibitor as a potential chemopreventive to UV-induced skin cancer, Arch Dermatol 138 (2002), pp. 751–755. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (55)
[3] R. Wolf, H. Matz, M. Zalish, A. Pollack and E. Orion, Prostaglandin analogs for hair growth: great expectations, Dermatol Online J 9 (2003) (3), p. 7. View Record in Scopus | Cited By in Scopus (6)
[4] M.R. Namazi, The beneficial and detrimental effects of linoleic acid on autoimmune disorders, Autoimmunity 37 (2004) (1), pp. 73–75. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (2)
[5] W.F. Bergfeld, Androgenetic alopecia:next term an autosomal dominant disorder, Am J Med 98 (1995) (Suppl. 1A), pp. 95S–98S.