TAILIEUCHUNG - Chapter 057. Photosensitivity and Other Reactions to Light (Part 3)

Vitamin D Photochemistry Cutaneous exposure to UV-B causes photolysis of epidermal 7dehydrocholesterol converting it to pre-vitamin D3, which then undergoes a temperature-dependent isomerization to form the stable hormone vitamin D3. This compound then diffuses to the dermal vasculature and circulates systemically where it is converted to the functional hormone 1,25-dihydroxyvitamin D3[1,25(OH)2D3]. Vitamin D metabolites from the circulation or those produced in the skin itself can augment epidermal differentiation signaling. Controversy exists regarding the importance of sun exposure in vitamin D homeostasis. At present, it is important to emphasize that the use of sunscreens does not substantially diminish vitamin D. | Chapter 057. Photosensitivity and Other Reactions to Light Part 3 Vitamin D Photochemistry Cutaneous exposure to UV-B causes photolysis of epidermal 7-dehydrocholesterol converting it to pre-vitamin D3 which then undergoes a temperature-dependent isomerization to form the stable hormone vitamin D3. This compound then diffuses to the dermal vasculature and circulates systemically where it is converted to the functional hormone 1 25-dihydroxyvitamin D3 1 25 OH 2D3 . Vitamin D metabolites from the circulation or those produced in the skin itself can augment epidermal differentiation signaling. Controversy exists regarding the importance of sun exposure in vitamin D homeostasis. At present it is important to emphasize that the use of sunscreens does not substantially diminish vitamin D levels. Since aging also substantially decreases the ability of human skin to photocatalytically produce vitamin D3 the widespread use of sunscreens that filter out UV-B has led to concern that vitamin D deficiency may become a significant clinical problem in the elderly. Chronic Effects of Sun Exposure Nonmalignant The clinical features of photodamaged sun-exposed skin consist of wrinkling blotchiness and telangiectasia and a roughened irregular weatherbeaten leathery appearance. Whether this photoaging represents accelerated chronologic aging or a separate and distinct process is not clear. Within chronically sun-exposed epidermis there is thickening acanthosis and morphologic heterogeneity within the basal cell layer. Higher but irregular melanosome content may be present in some keratinocytes indicating prolonged residence of the cells in the basal cell layer. These structural changes may help to explain the leathery texture and the blotchy discoloration of sun-damaged skin. UV-A is important in the pathogenesis of photoaging in human skin and ROS are likely involved. The dermis and its connective tissue matrix are the major site for sun-associated chronic damage manifest as solar .

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