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

Abstract

The therapeutic use of BAL (2,3-dimercaptopropanol) as treatment for poisoning has been halted by data suggesting serious neurotoxicity. This article is a report on the effects of BAL and other dithiols, DMSA (meso-2,3-dimercaptosuccinic acid) and DMPS (2,3-dimercaptopropane-1-sulfonic acid), on [3H]glutamate release and uptake by rat brain synaptosomes and [3H]glutamate uptake by synaptic vesicles. BAL (100 microM) inhibited glutamate uptake (30%) and stimulated its basal release (30%) in synaptosomes, without affecting K+-stimulated release. BAL also inhibited glutamate uptake by synaptic vesicles (up to 60%). DMPS and DMSA (100 microM) had no significant effects on these parameters. The data reported here provide some evidence of glutamate involvement in BAL-induced neurotoxicity by demonstrating direct effects of BAL on glutamatergic system modulation.

• Authors: C W Nogueira, L L Rotta, R G Tavares, D O Souza, J B Rocha
• Journal: Neuroreport (Neuroreport) Vol. 12 Issue 3 Pg. 511-4 (Mar 05 2001) ISSN: 0959-4965 [Print] England
• PMID: 11234755 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Chelating Agents
• Dimercaprol
• Tritium
• Glutamic Acid
• Unithiol
• Succimer
• Potassium

Topics

• Animals
• Biological Transport (drug effects)
• Brain (metabolism)
• Chelating Agents (toxicity)
• Dimercaprol (toxicity)
• Glutamic Acid (pharmacokinetics)
• In Vitro Techniques
• Male
• Potassium (pharmacology)
• Rats
• Rats, Wistar
• Succimer (toxicity)
• Synaptosomes (drug effects, metabolism)
• Tritium
• Unithiol (toxicity)