文献类型：期刊文献

英文题名：Tebufenozide induces G1/S cell cycle arrest and apoptosis in human cells

作者：Xu, Wenping[1];Wang, Bo[1];Yang, Mingjun[1];Zhang, Yang[1];Xu, Zhiping[1];Yang, Yun[1];Cao, Haijing[1];Tao, Liming[1]

机构：[1]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai 200237, Peoples R China

年份：2017

卷号：49

起止页码：89

外文期刊名：ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000393246600012)】；

基金：This work was financially supported by National Key Technology Research Development Program of China (NO.2011BAE06B04).

语种：英文

外文关键词：Pesticide; Tebufenozide; Cytotoxic effects; DNA damage; Cell cycle arrest; Apoptosis

摘要：Tebufenozide is a non-steroidal insect growth regulator and is extensively used to control pests, although it is considered to be safe for mammals and environmentally friendly. However, previous studies have found that tebufenozide is cytotoxic to man, although the exact mechanism remains elusive. This study will investigate the apoptotic molecular mechanisms which result from tebufenozide-induced DNA damage in HeLa cells. Our results demonstrate that tebufenozide could trigger arrest in G1/S phase related to a downregulation of cyclin E and cyclin-dependent kinase (CDK) 2 protein. In addition, Western blotting showed apoptosis was associated with the upregulation of p53, Bax and cleaved-PARP, as well as downregulation of Bcl-2 and PARP. Tebufenozide also regulated changes in mitochondrial permeability and reduced mitochondrial number and intracellular ATP production. Briefly, these results suggest that tebufenozide-induces cell cycle arrest and apoptosis through activating p53 protein in a Bax- and Bcl-2-triggered mitochondrial pathway. This work provides some scientific context for the safe use of tebufenozide in agriculture. (C) 2016 Elsevier B.V. All rights reserved.