Effects of arsenite on glutamate metabolism in primary cultured astrocytes

Abstract

The aim of this study was to explore the mechanisms that contribute to neurotoxicity induced by arsenite exposure focusing on the alteration of glutamate metabolism in primary cultured astrocytes. The cells were exposed to 0–30μM arsenite for 24h, and then cell viability, intracellular nonprotein sulfhydryl (NPSH) levels, mitochondrial membrane potential, activity of Na+/K+-ATPase, glutamine synthetase (GS) and glutamate transporter (GLAST and GLT-1), and protein expression of GS, GLAST and GLT-1 were examined. Compared with those in control, exposure to arsenite resulted in damages of astrocytes in a concentration dependent manner, which were shown by cell viabilities, and supported by morphological observation, mitochondrial membrane potential and intracellular NPSH levels. On the other hand, activities and protein expression of GS, GLAST and GLT-1 were significantly inhibited by arsenite exposure. Moreover, protein expression of GLAST and activities of GS were much more sensitive to arsenite. However, activities of Na+/K+-ATPase were not influenced obviously by arsenite exposure. In conclusion, findings from this study indicated that exposure to arsenite could inhibit glutamate metabolism in astrocytes, which might be related to arsenic-induced neurotoxicity.