INTRACELLULAR GLUTATHIONE (GSH) LEVELS MODULATE MERCURIC-CHLORIDE (MC)- AND METHYLMERCURIC CHLORIDE (MEHGCL)-INDUCED AMINO-ACID RELEASE FROM NEONATAL RAT PRIMARY ASTROCYTES CULTURES

Mercuric chloride (MC) and methylmercury (MeHg) were found to increase amino acid release from astrocytes. This suggests interaction with su lfhydryl (-SH) groups which are controlled by glutathione [GSH] levels . In the present study, we evaluated the effects of alterations in int racellular glutathione concentrations [GSH], on the outcome of MC and MeHg treatment. [GSH](i)l were increased in a time-dependent fashion b y incubating the astrocytes with 1 mM L-2-oxothiazolidine-4-carboxylic acid (OTC), a cysteine precursor. OTC attenuated the release of [2,3- H-3]D-aspartic acid from astrocytes exposed to MC-(5 mu M) and MeHg-(1 0 mu M). MeHg-induced [3H]D-taurine release was also reduced by pretre atment of astrocytes with OTC. Treatment with BSO (50 mu M) decreased [GSH], in astrocytes, and increased [2,3-H-3]D-aspartate release from MC- and MeHg-treated astrocytes, and [3H]D-taurine release from MeHg-t reated cells. Neither OTC nor BSO when added to cultures in the absenc e of MC or MeHg had an effect on amino acid release by astrocytes. The current study underscores both the sensitivity of astrocytes to mercu rials in terms of amino acid release and the relationship of these eff ects to astrocytic [GSH],.