Oxidative stress-independent depletion of epidermal vitamin A by UVA.
In hairless mice, epidermal vitamin A (retinol and retinyl esters) is strongly decreased following a single exposure to UVB. Here, using the same mouse model, we studied the effects of UVA on epidermal vitamin A content, lipid peroxidation, and CRBP-I expression, as well as the putative prevention of vitamin A depletion or lipid peroxidation by topical alpha-tocopherol. An acute exposure to UVA completely depleted epidermal vitamin A with EC50 of 0.25 and 0.5 J per cm2 for retinyl esters and retinol, respectively; these values were 0.1 J per cm2 for both retinoids under UVB exposure. CRBP-I expression was increased 2-fold 8 h following UVA exposure (10 J per cm2), and this increase persisted for at least 16 h. A single UVA exposure induced a concentration-dependent epidermal lipid peroxidation (EC50 = 3.5 J per cm2) giving rise to 55.4 +/- 4.2 nmol lipid peroxides per g at 20 J per cm2, whereas UVB, up to 1 J per cm2, did not increase the basal concentration of 6.7 +/- 0.9 nmol lipid peroxides per g. On the other hand, topical menadione induced a concentration-dependent lipid peroxidation, but did not affect vitamin A content. Pretreatment with alpha-tocopherol (i) did not inhibit UV-induced vitamin A depletion, (ii) completely inhibited the increased lipid peroxidation induced by UVA or menadione, and (iii) accelerated reconstitution of epidermal vitamin A after UVB but not UVA induced depletion. Thus acute UVA induced both epidermal vitamin A depletion and lipid peroxidation, UVB induced only vitamin A depletion, and menadione induced only a lipid peroxidation; topical alpha-tocopherol prevented lipid peroxidation but not vitamin A depletion. These observations indicate (i) that CRBP-I neither provides protection to UVB- and UVA-induced epidermal vitamin A depletion, nor interferes significantly with reconstitution, and (ii) that the UV-induced vitamin A depletion and lipid peroxidation in mouse epidermis are unrelated processes. UV light does not destroy epidermal vitamin A through an oxidative stress but probably by a photochemical reaction in which UV radiations at about 325 nm give the corresponding activation energy.
Sorg
Olivier
O
Department of Dermatology, University Hospital, Geneva, Switzerland. olivier.sorg@hcuge.ch
Tran
Christian
C
Carraux
Pierre
P
Didierjean
Liliane
L
Falson
Francoise
F
Saurat
Jean-Hilaire
JH
D000287:Administration, Topical; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology; D004817:Epidermis / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects*; D008054:Lipid Peroxides / Q000037:antagonists & inhibitors / Q000378:metabolism; D051379:Mice; D008812:Mice, Hairless; D018384:Oxidative Stress / Q000502:physiology*; D012176:Retinoids / Q000037:antagonists & inhibitors; D012177:Retinol-Binding Proteins / Q000378:metabolism; D054840:Retinol-Binding Proteins, Cellular; D014212:Tretinoin / Q000378:metabolism; D014466:Ultraviolet Rays; D014801:Vitamin A / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000528:radiation effects; D024483:Vitamin K 3 / Q000494:pharmacology; D024502:alpha-Tocopherol / Q000494:pharmacology
D000975:Antioxidants; D008054:Lipid Peroxides; D012176:Retinoids; D012177:Retinol-Binding Proteins; D054840:Retinol-Binding Proteins, Cellular; D014801:Vitamin A; D014212:Tretinoin; D024483:Vitamin K 3; D024502:alpha-Tocopherol