Mercury is a potent neurotoxin that can delay neurological development in neonates, and has been proposed to be an environmental risk factor for several neurodegenerative conditions. The mechanisms by which environmental factors may influence the propagation of neurodegenerative diseases are not yet well delineated. However, it is known that neurons require trophic factor support for maintenance and survival following traumatic physical and toxic insults. We found that divalent mercury (HgCl2) inhibited ciliary neurotrophic factor and interferon-g receptor– mediated Janus tyrosine kinase (Jak)/signal transducers and activators of transcription (STAT) pathway activation in SK-N-BE(2)-C neuroblastoma cell cultures, but did not inhibit the fibroblast growth factor receptor tyrosine kinase. Results of dichlorofluorescein experiments showed increased levels of oxidative stress in HgCl2-treated cells that was similar in magnitude to that cause
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