Vitamin A Homeostasis in Human Epidermis: Native Retinoid Composition and Metabolism

Vitamin A, or retinol, has long been known to play a critical role in epithelial homeostasis. Its importance in the maintenance of healthy epithelium was first recognized by Mori (1922) with the discovery that the cornea became keratinized in vitamin A deficient animals. Soon thereafter Wolbach and Howe (1925) documented the conversion of mucosal epithelial tissues to squamous, metaplastic, hyperkeratinized epithelia — epithelia resembling the epidermis — in vitamin A deficient rats. In the authors’ words,“… replacement of many different epithelia by stratified keratinizing epithelium actually characterize[s] fat-soluble A avitaminosis. The specific pathology is the widespread keratinization.” Indeed, even normal or orthokeratotic skin appeared to require vitamin A, as Frazier and Hu (1931) and Goodwin (1934) later described the cutaneous hyperkeratosis that accompanies vitamin A deficiency in human beings. In addition, the hyperkeratosis observed in vitamin A deficiency could be reversed by restoring vitamin A to the diet (Frazier and Hu 1931; Goodwin 1934). These early observations serve as the foundation for the idea that all epithelial tissues, including the epidermis, require adequate vitamin A nutritional status to sustain normal growth and differentiation.