Abstract

The generation of ROS and lipid peroxidation has been considered to play an important role in the pathogenesis of chronic fluoride toxicity. In the present study, we observed that fluoride activated BV-2 microglia cell line by observing OX-42 expression in immunocytochemistry. Intracellular superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), reactive oxygen species (ROS), superoxide anions (O(2)(?-)), nitric oxide synthase (NOS), nitrotyrosine (NT) and nitric oxide (NO), NOS in cell medium were determined for oxidative stress assessment. Our study found that NaF of concentration from 5 to 20 mg/L can stimuli BV-2 cells to change into activated microglia displaying upregulated OX-42 expression. SOD activities significantly decreased in fluoride-treated BV-2 cells as compared with control, and MDA concentrations and contents of ROS and O(2)(?-) increased in NaF-treated cells. Activities of NOS in cells and medium significantly increased with fluoride concentrations in a dose-dependent manner. NT concentrations also increased significantly in 10 and 50 mg/L NaF-treated cells compared with the control cells. Our present study demonstrated that toxic effects of fluoride on the central nervous system possibly partly ascribed to activiting of microglia, which enhanced oxidative stress induced by ROS and reactive nitrogen species.

Excerpt:

In conclusion, a main finding of this study was that microglia BV-2 cells were activated by fluoride, and the increase of ROS and RNS in microglia was associated with the activation of microglia. The novelty of this work is related to the active role of microglia treated with fluoride. We provided new evidence from in vitro model indicating that fluoride exerts its toxic effects in CNS possibly partly ascribed to activating of microglia in vitro, which enhanced oxidative stress induced by ROS and RNS. Of course, the detailed effect and mechanism need further investigation in vivo.

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*Original abstract online at https://www.hindawi.com/journals/mi/2012/102954/

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