Ultraviolet irradiation of human skin causes functional vitamin A deficiency, preventable by all-trans retinoic acid pre-treatment

Nat Med. 1999 Apr;5(4):418-22. doi: 10.1038/7417.

Abstract

We report here that ultraviolet irradiation substantially reduced the mRNA and protein of the two major nuclear retinoid receptors, RAR-gamma and RXR-alpha, in human skin in vivo. Pre-treatment with retinoic acid mitigated this loss of nuclear retinoid receptors. Ultraviolet irradiation caused a near-total loss of retinoic acid induction of two RAR/RXR target genes, cellular retinoic acid binding protein-II and RA 4-hydroxylase, but did not affect 1,25-dihydroxyvitamin D3 induction of the vitamin D receptor/RXR-regulated gene vitamin D 24-hydroxylase. In effect, ultraviolet irradiation causes a functional vitamin A deficiency that may have deleterious effects on skin function, contributing to skin photo-aging and carcinogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Topical
  • Adult
  • Biopsy
  • Cell Nucleus / radiation effects
  • Cytochrome P-450 Enzyme System / radiation effects
  • Humans
  • Male
  • Middle Aged
  • RNA, Messenger / radiation effects
  • Receptors, Calcitriol / metabolism
  • Receptors, Retinoic Acid / genetics
  • Receptors, Retinoic Acid / radiation effects
  • Retinoic Acid 4-Hydroxylase
  • Retinoid X Receptors
  • Skin / radiation effects*
  • Steroid Hydroxylases / radiation effects
  • Transcription Factors / genetics
  • Transcription Factors / radiation effects
  • Tretinoin / therapeutic use*
  • Ultraviolet Rays / adverse effects*
  • Vitamin A Deficiency / drug therapy*
  • Vitamin D3 24-Hydroxylase

Substances

  • RNA, Messenger
  • Receptors, Calcitriol
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Transcription Factors
  • retinoic acid binding protein II, cellular
  • Tretinoin
  • Cytochrome P-450 Enzyme System
  • Steroid Hydroxylases
  • Retinoic Acid 4-Hydroxylase
  • Vitamin D3 24-Hydroxylase