Poster
# 99
Poster |
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6th Internet World Congress for Biomedical Sciences |
Denise Lewis(1)
(1)Wake Forest University School of Medicine - Winston-Salem. United States
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Contact address: |
Denise Lewis Wake Forest University School of Medicine Medical center Blvd Winston-Salem NC 27157-1083 United States dlewis@wfubmc.edu |
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[Toxicology] |
Manganese (Mn) is an essential nutrient that, at excessive levels, produces extrapyramidal symptoms resembling those observed in patients with Parkinson´s disease. Because of the similarities in the symptoms of Mn toxicity (manganism) and Parkinson´s disease (related to dopamine depletion), Mn toxicity was tested in a cell line that produces catecholamines, CATH.a cells. Manganese was demonstrated to to be toxic (LD50 = 33 M) in the CATH.a cells after 24 hours exposure time. The toxicity produced by manganese in the CATH.a cells was augmented in glutathione reduced cells (LD50 = 1 M) by pretreating the cells for 36 hours with an inhibitor of glutathione synthesis, L-Buthionine sulfoximine (L-BSO)
In an attempt tp elucidate the mechanism of manganese´s toxicity, cells were exposed to 33 M Mn at a time point when Mn was less toxic (18 hours). RNA was isolated and used for a cDNA expression array, a tool used to look at the expression of a number of genes at one time.
Our results suggest a few things: 1) at 18 hours manganese upregulates a plethora of genes suggesting that exposing the cells to Mn for a shorter time point would be a more suitable method to help discern a method of action for its toxicity 2) Manganese could be involved in any number of pathways, from calcium related signal transduction pathways to apoptosis driven pathways. More follow up studies are needed to produce a more concrete pathway for manganese toxicity.
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[Toxicology] |
