Inhibition of the acute ocular responses to nitrogen mustard by colchicine

Colchicine, a naturally occurring alkaloid, inhibits both fast and slow axoplasmic transport by prevention of microtubule assembly. We have examined the influence of colchicine on the neurogenically mediated acute inflammatory responses to topically administered nitrogen mustard and formaldehyde on the albino rabbit eye. Topical administration of colchicine (10, 20 or 40 micrograms) once per day for 15 days inhibited the ocular hypertensive response, the leakage of protein into the anterior chamber, and the pupillary constriction observed following topical administration of nitrogen mustard. Colchicine pretreatment also inhibited the ocular hypertensive response to topically administered formaldehyde. Pretreatment of the eye with colchicine (20 micrograms day-1) for a period of 5 days proved to be ineffective in suppressing the ocular hypertensive effect of nitrogen mustard, while more prolonged pretreatment (10 or 15 days) significantly abrogated the characteristic injury responses. Topical administration of colchicine (20 and 40 micrograms) caused dilation of conjunctival and limbal vessels, but these vascular responses subsided as treatment continued. These preliminary experiments suggest that the inhibition of the ocular responses to nitrogen mustard by chronic colchicine pretreatment might be the result of modification of synthesis or release of sensory mediator(s).