A hypothetical mechanism for toxic cataract due to oxidative damage to the lens epithelial membrane.
Lenticular opacities can be induced by numerous external agents that coincide with those that catalyze oxidative damage to lipids. One of the consequences of lipid peroxidation is that the affected membrane is rendered more permeable to protons. A proton leak in the tight epithelium of lens would uncouple the Na+/K(+)-ATPases that regulate the water and ionic content of the bounded tissue. Once regulatory control of the osmotic pressure is lost, the phase state of the cell's soluble proteins would change, leading to refractive changes or, in extreme cases, precipitation. The same does not occur in cornea because the stroma is an extracellular polymer blend rather than solution of soluble polymers. Polymeric phase transitions in the cornea require that divalent cations pass the epithelial membrane, which can occur only through the action of ionophores.
Bender
C J
CJ
Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461.
D000818:Animals; D002386:Cataract / Q000209:etiology*; D002463:Cell Membrane Permeability; D003315:Cornea / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D006801:Humans; D007908:Lens, Crystalline / Q000378:metabolism*; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000633:toxicity; D008954:Models, Biological; D018384:Oxidative Stress; D010684:Philosophy
D008054:Lipid Peroxides