EN
Polychlorinated biphenyl (PCB) congeners and polibrominated fl ame retardants (BFRs) are environmentally occurring toxins that exhibit a broad range of adverse biological effects including neurotoxicity. Due to their stability and lipophilic character, they persist in the environment and accumulate in brain of animals and humans contributing to induction of neurological disorders. The mechanisms by which PCBs and BFRs cause neurotoxic effects are still not completely understood. However, it is postulated that glutamate excitotoxicity may be involved. The main glutamate transporters GLT-1 and GLAST are membrane-bound proteins localized in glial cells. The clearance of synaptically released glutamate by these proteins protects neurons from excitotoxicity. The aim of the study was to establish whether the chronic exposure to these substances may infl uence the expression and activity of main glutamate transporters in rat brain. Aroclor 1254 (PCBs) and tetrabromobisphenol A (BFRs) were administered by oral gavage, which resembles the human exposure through the food chain, for two weeks. Signifi cant changes in the expression of glutamate transporters were observed, especially in the case of GLT-1. The effect was more pronounced for Aroclor 1254. The results suggest that GLT-1 is a molecular target of this toxin that may, almost partially, contribute to PCBs-induced excitotoxicity. This study was supported by grant nr NN401024635 from Polish Ministry of Science and Higher Education.