Effects of Cetylpyridinium Chloride on the Membranes of the Lens Fibers and on Lens Permeability, Hydration and <sup>22</sup>Na and <sup>86</sup>Rb Transport

Abstract

Cetylpyridinium chloride (CPC) lysed the membranes of the lens fibers without damaging the lens capsule. Swelling of lens fibers preceded their rupture. The following chemical changes were found in lenses incubated in Tyrode’s media containing CPC: gain of Na⁺ ions and water with loss of K⁺ ions, increase in the total Na⁺ + K⁺ ions concentrations (osmolarity), (c) a 10-fold increase in the ²²Na space and 2.6-time increase in the ¹⁴C inulin space (4 h <i>in vitro</i>), (d) marked increases in ⁸⁶Rb and ²²Na lens permeability, (e) inactivation of the ²²Na and ⁸⁶Rb ‘pumps’. CPC exposure resulted in selective lysis of fibers (posterior lens surface) or fibers and epithelial cells (anterior lens surface). At the 0.1-percent CPC concentration, damage to the posterior lens surface increased ⁸⁶Rb permeability and stimulated the ⁸⁶Rb ‘pump’. When the anterior surface was damaged by CPC, the lens permeability to K⁺, Na⁺ or water was greater than when the posterior surface was damaged. Lactate formation <i>in vitro</i> was decreased only when the anterior surface of the lens was exposed to CPC. Na⁺ and K⁺ ions were distributed asymmetrically in the normal rabbit lens. CPC-induced cataracts, with Na⁺ ion gains and K⁺ ion losses were localized to the posterior lens cortex of the rabbit. Circumferential (along fibers) and translenticular movement of Na⁺ or K⁺ ions were present in the cataracts. Na⁺–K⁺ pump-leak by the lens involved systems which were differentiated at the individual fiber or regional level as well as the lens as a whole.