Abstract—: The ultraviolet (UV) B-induced damage of the eye surface of experimental animals (rabbits) includes total loss of corneal epithelium, apoptosis of keratocytes and stromal edema. These changes are accompanied by clinically and histologically manifested corneal inflammation, neutrophil infiltration, and exudation of the anterior chamber of the eye. According to results of mass spectrometric analysis, the UV-induced corneal damage is associated with pronounced changes in the tear lipid composition, including a decrease in the amount of arachidonic acid and prostaglandin E2 and an increase in the concentrations of prostaglandin D2 and its derivative 15d-PGJ2. In addition, it is accompanied by changes in the levels of hydroxyeicosate tetraenic acids, including a decrease of 12-HETE and an increase of 5-HETE. These changes suggest activation of metabolic pathways involving 5-lipoxygenase, 12-lipoxygenase, cyclooxygenases 1 and 2, and prostaglandin D synthase. These findings contribute to understanding mechanisms of UV-induced keratitis and point to feasibility of selective anti-inflammatory therapy for improving corneal regeneration after iatrogenic UV damage. © 2019, Pleiades Publishing, Ltd.