Deoxynivalenol induces apoptosis in PC12 cells via the mitochondrial pathway

被引：44

作者：

Wang, Xichun ^{[1
]}

Xu, Wei ^{[1
]}

Fan, Mengxue ^{[1
]}

Meng, Tingting ^{[1
]}

Chen, Xiaofang ^{[1
]}

Jiang, Yunjing ^{[1
]}

Zhu, Dianfeng ^{[1
]}

Hu, Wenjuan ^{[1
]}

Gong, Jiajie ^{[1
]}

Feng, Shibin ^{[1
]}

Wu, Jinjie ^{[1
]}

Li, Yu ^{[1
]}

机构：

[1] Anhui Agr Univ, Coll Anim Sci & Technol, 130 West Changjiang Rd, Hefei 230036, Anhui, Peoples R China

来源：

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2016年 / 43卷

基金：

中国国家自然科学基金;

关键词：

Deoxynivalenol; Cytotoxicity; Neurotoxicity; Apoptosis; PC12; cell; MYCOTOXIN CONTAMINATION; OXIDATIVE STRESS; INDUCTION; GENOTOXICITY; ACTIVATION; VOMITOXIN; CEREALS; CALCIUM; NEURONS; FAMILY;

D O I：

10.1016/j.etap.2016.03.016

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

Deoxynivalenol (DON) has broad toxicity in animals and humans. In this study the impact of DON treatment on apoptotic pathways in PC12 cells was determined. The effects of DON were evaluated on (i) typical indicators of apoptosis, including cellular morphology, cell activity, lactate dehydrogenase (LDH) release, and apoptosis ratio in PC12 cells, and on (ii) the expression of key genes and proteins related to apoptosis, including Bcl-2, Box, Bid, cytochrome C (Cyt C), apoptosis inducing factor (AIF), cleaved-Caspase9, and cleaved-Caspase3. DON treatment inhibited proliferation of PC12 cells, induced significant morphological changes and apoptosis, promoted the release of Cyt C and AIF from the mitochondria, and increased the activities of cleaved-Caspase9 and cleaved-Caspase3. Bcl-2 expression decreased with increasing DON concentrations, in contrast to Box and Bid, which were increased with increasing DON concentration. These data demonstrate that DON induces apoptosis in PC12 cells through the mitochondrial ;apoptosis pathway. (C) 2016 Elsevier B.V. All rights reserved.

引用

页码：193 / 202

页数：10

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