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Ultraviolet irradiation depletes cellular retinol and alters the metabolism of retinoic acid in cultured human keratinocytes and melanocytes

Andersson, Eva, 1946- (author)
Linköpings universitet,Dermatologi,Hälsouniversitetet
Rosdahl, Inger, 1943- (author)
Linköpings universitet,Dermatologi,Hälsouniversitetet
Törmä, Hans (author)
Uppsala universitet,Institutionen för medicinska vetenskaper,Dermatology and Venereology,Department of Medical Sciences, Sect. of Dermatol. and Venereology, Uppsala University, Uppsala, Sweden
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Vahlquist, Anders (author)
Uppsala universitet,Institutionen för medicinska vetenskaper,Dermatology and Venereology,Department of Medical Sciences, Sect. of Dermatol. and Venereology, Uppsala University, Uppsala, Sweden
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 (creator_code:org_t)
1999
1999
English.
In: Melanoma research. - 0960-8931 .- 1473-5636. ; 9:4, s. 339-346
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Vitamin A is an intrinsic modulator of proliferation and differentiation in human epidermis, and may be destroyed by ultraviolet radiation (UVR) impinging on the skin. To identify the deleterious effects of a perturbed cellular vitamin A status, we investigated the endogenous retinoid concentrations and the metabolism of [3H]retinol and all-trans [3H]retinoic acid in cultured human keratinocytes and melanocytes exposed to UVR, using high performance liquid chromatography. Before UVR the retinoid content was similar in keratinocytes and melanocytes, but the uptake of [3H]retinol was three-fold higher and the uptake of [3H]retinoic acid was 10-fold higher in the melanocytes. In both cell types, UVR (UVA 360 mJ/cm2 plus UVB 140 mJ/cm2) instantaneously reduced the concentration of retinol by about 50% and that of 3,4-didehydroretinol by about 20%. The retinoid concentrations returned to normal within 1-2 days post-irradiation, despite there being no overt increase in the uptake of [3H]retinol or the biosynthesis of 3,4-didehydroretinol. However, in both types of irradiated cells, the accumulation of the biologically most active metabolite, all-trans [3H]retinoic acid, was about 60% higher than in control cells. Furthermore, the metabolism of authentically supplied [3H]retinoic acid was reduced, especially in irradiated keratinocytes, which probably contributed to the restoration of retinoid levels after UV exposure.

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