[The role of tear acidity and Cu-cofactor of lysyl oxidase activity in the pathogenesis of keratoconus].

Detailed analysis of copper compounds migration in the corneal stroma are presented. The biochemical conditions of the middle periphery of the cornea is found to inhibit copper ions movement to the center in patients with keratoconus due to increased tear alkalinity. Low concentration of dichlorocuprate (I) ion in the center of cornea results in inactivation of lysyl oxidase, an enzyme that catalyzes collagen cross-linking, and thus promotes keratoconus. Revealed association of tear acidity and copper distribution in cornea offers new opportunities in pathogenic treatment of keratoconus.