cholecalciferol and Sunburn

Vitamin D is generally accepted in its importance on the regulation of calcium homeostasis and bone metabolism. Moreover, further health effects due to vitamin D are under discussion. In its effect, vitamin D is more like a hormone. In the classic view, a vitamin is an essential nutrient, which cannot be synthesized independently in the body. Besides nutrition, vitamin D will be produced in the body itself. The skin contains the provitamin D3 7-dehydrocholesterol, a precursor of vitamin D. Provitamin D3 will be photoconverted to previtamin D3 by UVB radiation that penetrates the skin superficially. In this way, the vitamin D metabolism will be started independent of the nutrition. In everyday life, this photosynthesis will be carried out due to the solar UVB radiation penetrating the uncovered skin. In the same spectral waveband range of UVB radiation, which causes the beneficial health effect of starting the vitamin D metabolism, the UVB radiation causes simultaneously acute and chronic harmful health effects as UV erythema (sunburn), skin aging and skin cancer. There is no vitamin D production in the skin without simultaneous DNA damage in the skin. Against this background, risks and benefits have to be balanced carefully.

Topics: Cholecalciferol; Dehydrocholesterols; Humans; Metabolic Networks and Pathways; Skin; Skin Aging; Skin Neoplasms; Sunburn; Ultraviolet Rays; Vitamin D

Cumulative ultraviolet exposure plays a critical role in photodamage. Recent advancements in photomedicine have resulted in a more thorough understanding of these mechanisms. Despite this, the adoption of routine sun protective practices is commonly not undertaken regularly by a large proportion of the public. Various obstacles exist that contribute to the public's nonadherence to these practices. Sunscreens, which are an integral component in all photoprotective regimens, have been questioned recently in terms of their safety. The aim of this article is to provide an overview of new concepts in photoprotection and also address current controversies pertaining to sunscreens.

Topics: Antioxidants; Benzophenones; Cholecalciferol; Coral Reefs; Deoxyribodipyrimidine Photo-Lyase; Endocrine Disruptors; Environment; Free Radicals; Humans; Pyrimidine Dimers; Skin Aging; Skin Neoplasms; Sun Protection Factor; Sunburn; Sunlight; Sunscreening Agents; Titanium; Ultraviolet Rays; Vitamins; Zinc Oxide

Topics: Cholecalciferol; DNA Repair; Eye; Female; Humans; Male; Melanoma; Neoplasms, Radiation-Induced; Skin; Skin Aging; Skin Neoplasms; Sunburn; Sunlight; Ultraviolet Rays

The diverse immunomodulatory effects of vitamin D are increasingly being recognized. However, the ability of oral vitamin D to modulate acute inflammation in vivo has not been established in humans. In a double-blinded, placebo-controlled interventional trial, 20 healthy adults were randomized to receive either placebo or a high dose of vitamin D

Topics: Administration, Oral; Adult; Cholecalciferol; Dose-Response Relationship, Drug; Double-Blind Method; Female; Follow-Up Studies; Humans; Inflammation; Male; Middle Aged; Skin; Sunburn; Time Factors; Treatment Outcome; Vitamins; Young Adult

Topics: Adult; Child; Child, Preschool; Cholecalciferol; Humans; Infant; Melanoma; Skin Neoplasms; Sunburn; Sunscreening Agents

Our in vitro studies demonstrate that normal human epidermal melanocytes become swollen and more dendritic with an increase in amount of immunoreactive tyrosinase when they are cultured for several days with arachidonic acid metabolites, vitamin D3 or histamine. From these data we propose the following possible mechanisms for hyperpigmentations noted at postinflammatory sites and suntanned areas as well as at skin lesions of urticaria pigmentosa. Arachidonic acid metabolites and histamine, which are found in increased amounts in inflammatory skin, are thought to play a key role in the induction of postinflammatory hyperpigmentation. In sunburnt skin the increased proinflammatory mediators, particularly arachidonic acid metabolites, are also thought to stimulate melanocytes in the production of hyperpigmentation. Thus tanning after sun exposure may be induced not only by the effect of vitamin D3 and direct UV irradiation on the melanocytes but also by the effect of various arachidonic acid metabolites which are increased in sunburnt skin. Mast cells massively proliferate in the skin lesions of urticaria pigmentosa. Thus hyperpigmentation in the skin lesions of urticaria pigmentosa is quite likely to be induced by the chemical mediators, including histamine and leukotrienes, that are released from these cells.

Topics: Arachidonic Acids; Cells, Cultured; Cholecalciferol; Histamine; Humans; Inflammation; Melanins; Melanocytes; Skin; Skin Pigmentation; Sunburn; Time Factors; Urticaria Pigmentosa