BAL modulates glutamate transport in synaptosomes and synaptic vesicles from rat brain

The therapeutic use of BAL (2.3-dimercaptopropanol) as treatment for poison ing has been halted by data suggesting serious neurotoxicity. This article is a report on the effects of BAF and other dithiols, DMSA (meso-2,3-dimerc aptosuccinic acid) and DMPS (2,3-dimercaptopropane-I-sulfonic acid), on [H- 3]glutamate release and uptake by rat brain synaptosomes and [H-3]glutamate uptake by synaptic vesicles. BAL (100 muM) inhibited glutamate uptake (30% ) and stimulated its basal release (30%) in synaptosomes, without affecting K+-stimulated release. BAL also inhibited glutamate uptake by synaptic ves icles (up to 60%). DMPS and DMSA (100 muM) had no significant effects on th ese parameters. The data reported here provide some evidence of glutamate i nvolvement in BAL-induced neurotoxicity by demonstrating direct effects of BAL on glutamatergic system modulation. NeuroReport 12:511-514 (C) 2001 Lip pincott Williams & Wilkins.