LAUSR

Mercury (Hg) is widely known by its neurotoxicity albeit immunotoxicity occurs at lower exposure levels. Since microglia cells are the major representatives of the immune system in the CNS, we hypothesize Hg compounds disrupt microglia homeostasis by interfering with the redox regulation of the NF-kB pathway. Thus, the goal of this work is to study the effect of Hg compounds on p50 and p65 activation, translocation and DNA binding, considering the interaction of Hg with the glutathione system. N9 mouse microglia cells were used as the experimental model and following exposure to different Hg compounds (Hg2+, EtHg and MeHg), cells were analyzed for GSH activity (DTNB assay), Grx oxidation state (redox western blot), nuclear translocation of p50 and p65 (Western blot) and expression (mRNA) of pro-inflammatory (e.g.IL1-s; TNF-α) markers. Results show GSH depletion is an early event during exposure of microglia to Hg in spite its high basal levels. We also examine how this decrease in available GSH is associated to enhanced translocation of p50 and p65 to the nucleus and activation of target gene transcription.