文献类型：期刊文献

英文题名：Spinosad induces programmed cell death involves mitochondrial dysfunction and cytochrome C release in Spodoptera frugiperda Sf9 cells

作者：Yang, Mingjun[1];Wang, Bo[1];Gao, Jufang[2];Zhang, Yang[1];Xu, Wenping[1];Tao, Liming[1]

机构：[1]East China Univ Sci & Technol, Shanghai Key Lab Chem Biol, Sch Pharm, Shanghai 200237, Peoples R China;[2]Shanghai Normal Univ, Coll Life & Environm Sci, Shanghai 200234, Peoples R China

年份：2017

卷号：169

起止页码：155

外文期刊名：CHEMOSPHERE

收录：;EI(收录号：20164803068848);WOS:【SCI-EXPANDED(收录号:WOS:000393003300019)】；

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

语种：英文

外文关键词：Spinosad; Programmed cell death; Mitochondrial dysfunction; Cytochrome C release

摘要：Spinosad, a reduced-risk insecticide, acts on the nicotinic acetylcholine receptors and the gamma-aminobutyric acid receptor in the nervous system of target insects. However, its mechanism of action in non-neural insect cells is unclear. This study aimed to evaluate mitochondrial functional changes associated with spinosad in Spodoptera frugiperda (Sf9) insect cells. Our results indicate that in Sf9 cells, spinosad induces programmed cell death and mitochondrial dysfunction through enhanced reactive oxygen species production, mitochondrial permeability transition pore (mPTP) opening, and mitochondrial membrane potential collapse, eventually leading to cytochrome C release and apoptosis. The cytochrome C release induced by spinosad treatment was partly inhibited by the mPTP inhibitors cyclosporin A and bongkrekic acid. Subsequently, we found that spinosad downregulated Bcl-2 expression and upregulated p53 and Bax expressions, activated caspase-9 and caspase-3, and triggered PARP cleavage in Sf9 cells. These findings suggested that spinosad-induced programmed cell death was modulated by mitochondrial dysfunction and cytochrome C release. (C) 2016 Elsevier Ltd. All rights reserved.