Title: Attenuation of Methylmercury‐induced Neurotoxicity by N‐methyl‐D‐aspartate Antagonist, MK801 in SH‐SY5Y Cells
Abstract: Methylmercury (MeHg), a well known neurotoxin, has been reported to alter glutamate homeostasis in the neuronal environment resulting in excitotoxicity. The present study was conducted to investigate whether, and if so, under what conditions, MeHg induced excitotoxicity may be attenuated by N‐methyl‐D‐aspartate (NMDA) receptor blockade. A cell viability tissue culture assay was utilized to study the effects of MeHg, glutamate (glu) and a non‐competitive NMDA antagonist, MK‐801 on a human neuroblastoma cell line, SH‐SY5Y. Treatment of cells with MeHg (50nM) and glu (1mM) alone demonstrated a decrease of cell viability from control of 64%±6.5 and 79%±8.5, respectively. When glu and MeHg were added to cells in combination there was a 45% decrease in cell viability (p<0.005 n=3), as compared to treatment of glu alone. MK‐801 (4μM) significantly protected the cells from the effects of glu alone (p<0.005 n=3) as well as from combination treatments with glu and MeHg (p<0.0001 n=3). This study indicates that MeHg may induce an increase in number of NMDA receptors on the cell surface of neuroblastoma cells, and thus enhance the toxicity of glutamate. This apparent blockade of NMDA receptor with MK801 demonstrated a significant attenuation of the toxicity of both MeHg and glutamate. These results support the hypothesis that NMDA receptor antagonists may provide a potential treatment for MeHg‐induced neurological diseases.
Publication Year: 2010
Publication Date: 2010-04-01
Language: en
Type: article
Indexed In: ['crossref']
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