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HL Kern, RW Bellhorn and CM Peterson
Ocular lesions secondary to sodium cyanate administration in the beagle are described. Fifteen dogs were given sodium cyanate at doses of 30 to 170 mg/kg/day, 5 days per week. Fourteen developed cataracts which were generally posterior and subcapsular. Five animals developed corneal lesions. Control beagles and cyanate-treated rats and monkeys did not develop lesions. The one drug-treated beagle without ocular lesions received a maximum dose of 30 mg/kg/day of sodium cyanate for 19 months and achieved a mean carbamylatin of 0.39 residue of cyanate per mol of hemoglobin. Animals developing cataracts received a maximum dose of 119+/-23 mg/kg/day for 28+/-10 months and achieved a mean carbamylation of 0.69+/-0.13 residue/mol. Animals developing corneal lesions received a maximum dose of 113+/-22 mg/kg/day for 36+/-7 months and achieved a mean carbamylation of 0.78+/-0.09 residue/mol. Younger animals appeared more susceptible to the cataractogenic effects of the drug than older ones. Lens intracellular sodium was increased by 100% in the cataractous lenses while potassium was significantly decreased in the lenses with the greatest opacity. Extracellular space was increased in the cataractous lenses by 61%. Reduced glutathione levels were decreased by 34% and lactate leakage into the medium was increased by 12%. Rubidium-86 uptake was increased by 26% in the cataractous lenses, probably reflecting an inadequate compensatory response to increased passive fluxes of cations resulting from a structural or enzymatic lesion.