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pubmed-article:12782102pubmed:abstractTextMethylmercury is known to have devastating effects on the mammalian nervous system. In order to characterize the dose dependence of methylmercury-induced neurotoxicity, we first studied neurite outgrowth from rat dorsal root ganglia explants. In this model, methylmercury inhibited neurite outgrowth with a TD(50) of approximately 0.5 microM. We then used this relationship to optimize dosing for subsequent transcriptional profiling analyses in two independent neuronal model systems: dissociated sensory neurons and PC12 cells. As seen in previous studies, the expression of a number of genes associated with oxidative stress was altered following a 6h challenge with 1 microM methylmercury. When PC12 cells were subjected to a longer exposure (24h), a relative increase was noted in the representation of genes associated with cell cycling and apoptosis. To confirm the presence of apoptosis in cultured neurons, we then applied TUNEL staining and bis-benzimide staining techniques to primary cultures of dissociated sensory neurons. After 24h, 1 microM methylmercury increased both DNA end-labeling (P<0.01) and nuclear fragmentation (P<0.02). The latter effect appeared to be dose-dependent.lld:pubmed
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pubmed-article:12782102pubmed:pagination369-78lld:pubmed
pubmed-article:12782102pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:12782102pubmed:year2003lld:pubmed
pubmed-article:12782102pubmed:articleTitleMethylmercury induces apoptosis in cultured rat dorsal root ganglion neurons.lld:pubmed
pubmed-article:12782102pubmed:affiliationPersonalized Medicine Center, Marshfield Medical Research Foundation, Marshfield Clinic, Marshfield, WI, USA.lld:pubmed
pubmed-article:12782102pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12782102pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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