Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 현동훈 | * |
dc.date.accessioned | 2016-08-28T12:08:29Z | - |
dc.date.available | 2016-08-28T12:08:29Z | - |
dc.date.issued | 2011 | * |
dc.identifier.issn | 0161-813X | * |
dc.identifier.other | OAK-8138 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222087 | - |
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. © 2011. | * |
dc.language | English | * |
dc.title | Fluazinam-induced apoptosis of SH-SY5Y cells is mediated by p53 and Bcl-2 family proteins | * |
dc.type | Article | * |
dc.relation.issue | 6 | * |
dc.relation.volume | 32 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 702 | * |
dc.relation.lastpage | 710 | * |
dc.relation.journaltitle | NeuroToxicology | * |
dc.identifier.doi | 10.1016/j.neuro.2011.08.004 | * |
dc.identifier.wosid | WOS:000297000400003 | * |
dc.identifier.scopusid | 2-s2.0-80055091982 | * |
dc.author.google | Lee J.E. | * |
dc.author.google | Kang J.S. | * |
dc.author.google | Shin I.C. | * |
dc.author.google | Lee S.-J. | * |
dc.author.google | Hyun D.-H. | * |
dc.author.google | Lee K.S. | * |
dc.author.google | Koh H.C. | * |
dc.contributor.scopusid | 현동훈(7005049041) | * |
dc.date.modifydate | 20240123112641 | * |