Abstract

The purpose of this study is to evaluate possible toxic effects of β-aminopropionitrile fumarate (βAPN), a lathyrogenic agent that inhibits fibrosis. This drug has been considered for use as an adjunct to surgical repair after topical application upon peripheral and central nervous system structures. In vivo and in vitro studies were done using rats to study the dose dependent neurotoxicity of this water soluble chemical. The results indicate that when the neural sheaths are removed the amplitude of the evoked sciatic nerve potential is irreversibly suppressed from 1 to 10 mM concentrations of βAPN. Nerve conduction velocities are relatively less affected with reduction from 43 to 35 m/sec by βAPN immersion. Similarly, the spinal cord studies show that when the dura and arachnoid are opened and damaged, 0.1 mM βAPN causes increased latency (from 9.9 to 14.5 msec) and decreased amplitude (from 79.4 to 56.8 μV) of cortical somatosensory evoked potentials. Possible mechanisms for the neurotoxic effects of βAPN are discussed.

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