| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5859647 | Toxicology | 2011 | 10 Pages |
Abstract
⺠Olaquindox caused cell cycle arrest to the S phase and induced cell apoptosis in HepG2 cells. ⺠Activation of mitochondrial pathways was established by determining the activity of initiator/effector caspases, the levels of PARP, p53 and Bcl-2 family proteins, and the release of cytochrome C from mitochondria. ⺠The results provide a mechanism approach in understanding the characterize of liver damage caused by olaquindox in vitro.
Keywords
DMEMFBSDCQp53qPCRHepG2human hepatocellular liver carcinoma cell lineBcl-2PARPΔΨmMPTPDMSODulbecco's modified Eagle's mediummitochondria permeability transition poreOlaquindoxTerminal deoxynucleotidyl transferase-mediated dUTP nick end labelingTUNELApoptosisdimethyl sulphoxidefetal bovine serumMitochondrial pathwayquantitative polymerase chain reactionMitochondrial membrane potentialPoly(ADP-ribose) polymerase
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Authors
Jiajie Zou, Qian Chen, Xi Jin, Shusheng Tang, Kaipao Chen, Ting Zhang, Xilong Xiao,