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The ultraviolet (UV) B-induced damage of the eye surface of experimental animals (rabbits) includes 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 mass spectrometric analysis, UV-induced corneal damage is associated with pronounced changes  in the lipid composition of tears, 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 an alteration in the levels of hydroxyeicosate tetraenic acid derivatives, namely upregulation of 12-HETE and  downregulation of 5-HETE. The revealed changes indicate the activation of metabolic pathways involving  5-lipoxygenase, 12-lipoxygenase, cyclooxygenase 1 and 2, and prostaglandin-D-synthase. These findings contribute  to understanding mechanisms of UV-induced keratitis and point on feasibility of selective anti-inflammatory therapy  for improving corneal regeneration after iatrogenic UV damage.

Inflammatory metabolites of arahidonic acid in tear fluid in UV-induced corneal damage