Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 신인철 | - |
dc.date.accessioned | 2018-04-12T13:39:16Z | - |
dc.date.available | 2018-04-12T13:39:16Z | - |
dc.date.issued | 2011-12 | - |
dc.identifier.citation | NeuroToxicology, 2011, 32(6), P.702-710 | en_US |
dc.identifier.issn | 0161-813X | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S0161813X11001331?via%3Dihub | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/65716 | - |
dc.description.abstract | A number of epidemiological studies have demonstrated a strong association between the incidence of neurodegenerative disease and pesticide exposure. Fluazinam (FZN) is a preventative fungicide from the pyridinamine group that was introduced in the 1990s and that quickly established itself as a new standard for the control of blight caused by Phytophthora infestans in potatoes. We used human neuroblastoma SH-SY5Y cells to investigate mechanisms of neuronal cell death in response to FZN and showed that FZN was cytotoxic to SH-SY5Y cells in a concentration- and time-dependent manner. Additionally, we showed that FZN treatment significantly decreased the neuron numbers including dopaminergic neurons and mitochondrial complex I activity. The cytotoxic effects of FZN were associated with an increase in reactive oxygen species (ROS) generation because pretreatment with N-acetyl cysteine, an anti-oxidant, reduced cell death. We showed that neuronal cell death in response to FZN was due to apoptosis because FZN increased cytochrome C release into the cytosol and activated caspase-3 through the accumulation of p53. FZN also reduced the levels of Bcl-2 protein but increased the levels of Bax. Our results provide insight into the molecular mechanisms of FZN-induced apoptosis in neuronal cells. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Elsevier Science B.V., Amsterdam. | en_US |
dc.subject | Fluazinam | en_US |
dc.subject | Apoptosis | en_US |
dc.subject | Reactive oxygen species | en_US |
dc.subject | p53 | en_US |
dc.subject | Bcl-2 family | en_US |
dc.title | Fluazinam-induced apoptosis of SH-SY5Y cells is mediated by p53 and Bcl-2 family proteins | en_US |
dc.type | Article | en_US |
dc.relation.no | 6 | - |
dc.relation.volume | 32 | - |
dc.identifier.doi | 10.1016/j.neuro.2011.08.004 | - |
dc.relation.page | 702-710 | - |
dc.relation.journal | NEUROTOXICOLOGY | - |
dc.contributor.googleauthor | Lee, J. E. | - |
dc.contributor.googleauthor | Kang, J. S. | - |
dc.contributor.googleauthor | Shin, I. C. | - |
dc.contributor.googleauthor | Lee, S. J. | - |
dc.contributor.googleauthor | Hyun, D. H. | - |
dc.contributor.googleauthor | Lee, K. S. | - |
dc.contributor.googleauthor | Koh, H. C. | - |
dc.relation.code | 2011207057 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | icshin | - |
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