Pathogenic features of acute ultraviolet-induced skin damage

This review describes the complex morphological, cellular, molecular and vascular changes that occur in the skin in the early period after ultraviolet (UV) exposure. The immediate effect of UV exposure is acute nonspecific damage to the skin, which is clinically expressed as UV erythema. When exposed to UV, a thickening of the epidermis occurs, along with spongiosis of keratinocytes, the formation of burn cells, a decrease in the Langerhans cell population, mast cell degranulation, vascular endothelium vasodilation, vasodilation, vasoactive substances — histamine, nitric oxide, arachidonic acid derivatives, which also contribute to the formation of infiltration of immune cells in the affected area. In addition, UV-induced damage to proteins and DNA molecules (forming dimers, crosslinks, photohydration products) develop and accumulate in skin cells, which ultimately leads to their apoptosis or to the start of carcinogenesis mechanisms. Radiation-induced peroxidation of membrane lipids by active oxygen radicals may contribute to the uptake of phospholipases. However, not all the mechanisms of acute UV damage to the skin that trigger the clinical erythema response are fully understood. New pathogenesis data may be of practical value and be used to personalize the determination of the minimum erythemal dose in phototherapy of various diseases. A detailed study of the pathological changes induced by UV contributes to the future development of new methods for the prevention of photoaging and carcinogenesis. At the global level, this will reduce mortality from malignant skin tumors, improve the results of phototherapy, optimize treatment costs and reduce the burden on medical personnel.