CORNEAL ENDOTHELIAL PERMEABILITY AFTER SILICONE OIL EXPOSURE - ROLE OF LOW-MOLECULAR-WEIGHT COMPONENTS AND CATALYST

Silicone oils induce corneal and retinal pathologic changes by undefined mechanisms that may relate to certain components. Low-molecular-weight components have often been postulated to cause these ocular toxicities. Several types of additives that occur as contaminants or by-products in crude silicone oils were tested for their effects on rabbit corneal endothelial permeability. A purified oil plus various additives was perfused to fill about 75% of anesthetized rabbit anterior chambers. In vitro endothelial permeabilities to inulin and dextran were determined after 1 week. A long-chain silanol-terminated polydimethylsiloxane (viscosity, 1000 cps) at 2 mg/ml, a catalyst (tetramethylammonium siloxamplate) at l mg/ml, and a mixture of a series of linear compounds (hexamethyldisiloxane [MM] through hexacosamethyldodecasiloxane [MD(10)M]) each at 10 mg/ml, resulting in the largest permeability increase. A mixture of two short-chain silanol-terminated compounds (15-35 cps plus 80 cps, each at 1 mg/ml) was less damaging, while the cyclic series gave ambiguous results. One series of hexamethylcyclotrisiloxane (D3), octamethylcyclotetrasiloxane (D4), and decamethylcyclopentasiloxane (D5) produced a modest increase in permeability, while another identical series from a different supplier had no effect and a mixture of a long series of various cyclic compounds from D3-D21 was without effect. Certain compounds have greater potential to induce toxic effects on the corneal endothelium including a linear series, a silanol-terminated polydimethylsiloxane, and a catalyst. Toxicity could reside in relatively few compounds; of these the linear series and the catalyst have been identified in silicone oils.