Corneas Of Dogs Research Articles

Ocular effects in dogs and pigs treated with dichloran (2.6-dichloro-4-nitroaniline)

Beagle dogs and miniature swine were fed dichloran (2.6-dichloro-4-nitroaniline) at levels of 0.75, 6.0, 24, 48 or 192 mg/kg/day in the diet for periods of 50–306 days. Corneal opacities appeared in the eyes of dogs given the 24- or 48-mg levels in 53–104 days in animals exposed to sunlight. Dogs unexposed to the light or with one eyelid sutured in the closed position failed to develop lesions in the unexposed eye or eyes. Slit-lamp examinations revealed that the corneal changes were located in the anterior corneal stroma just below the epithelium. Lens damage was confined to the central anterior cortical areas, giving a circular plaque appearance. These lesions were not reversible when the compound was withdrawn from the diet. Paraffin sections of the damaged corneas of dogs showed, when stained with haematoxylin and eosin, small yellow globules associated with the superficial corneal stromal-cell nuclei. Frozen sections stained with Oil Red O and toluidine blue revealed the globules as light-to-dark orange droplets. These droplets were more numerous in the group given 48 mg/kg/day but could also be observed in the groups given 6.0 and 0.75 mg/kg/day. The eyes of swine were unaffected by the feeding of dichloran at the dietary levels that were fed to dogs. Heinz bodies were present in the red blood cells of both dogs and swine given dichloran. Other toxic manifestations were not present in either species, except in the group of dogs given 192 mg/kg/day.

An experimental study of dichloroethane poisoning.

Systemic administration of 1, 2-dichloroethane causes corneal clouding specifically in the dog, but its lethality is approximately equivalent in dogs, cats, rabbits, and rats. In contrast to the ocular effects on systemic administration, injection of dichloroethane into the anterior chamber is equally toxic to the corneas of dogs, cats, and rabbits. The characteristic abnormality resulting from acute exposure, however administered, is a necrosis of the corneal endothelium beginning in the basal portion of the cells, secondary swelling of the stroma, formation of excess basement membrane and thickening of Descemet's layer, and repair by sliding or stretching of the surviving endothelial cells.